The document provides an overview of the immune system, including its components, cells, tissues, organs, and response mechanisms. It discusses the innate and adaptive immune responses, antigen recognition by innate immune cells and lymphocytes, maturation and activation of B and T cells, and the effector mechanisms that eliminate antigens. The major topics covered include pattern recognition receptors, antigen processing and presentation, T and B cell receptors, antibody production, signal transduction pathways, and the roles of phagocytes, dendritic cells, natural killer cells, and T cell subsets in the immune response.
The roles of the white blood cell subset γδ t cells within the human body are yet to be fully described.
Current literature has detailed several critical functions that vary dramatically between different γδ t cells.
Understanding how these elusive cells influence our immune systems will provide an opportunity to utilise their functions to assist medical treatments for a range of pathologies including cancer, diabetes, and bacterial infections.
Please send correspondence to Philip Voyias at P.D.Voyias@Warwick.ac.uk.
The document provides an overview of the immune system, including:
1) It describes the immune system as a complex, tiered system that distinguishes self from non-self via major histocompatibility complexes (MHCs) and recognizes antigens through both innate and adaptive responses.
2) The adaptive immune response involves an afferent limb for antigen recognition and presentation and an efferent limb that elicits effector responses through T cells, B cells, cytokines and antibodies.
3) Organ transplant rejection can occur via direct recognition of donor MHCs or indirect recognition of donor MHC fragments, with acute rejection being the most common type of allograft response.
Regulatory T cells (Tregs) play an important role in maintaining immune tolerance and suppressing excessive immune responses. Tregs can develop naturally in the thymus or be induced in the periphery. They express the transcription factor FoxP3 and surface markers CD4 and CD25. Tregs suppress the activation and functions of other immune cells and help prevent autoimmunity, control infections, allow transplantation tolerance, and support fetal-maternal tolerance in pregnancy. Dysregulation of Tregs has been linked to immunological diseases. Therapeutic use of Tregs may help treat diseases driven by excessive immune responses like autoimmunity.
This document provides an overview of mucosal-associated invariant T cells (MAIT). It discusses that MAIT cells are a type of innate alpha beta T cell that express a semi-invariant T cell receptor and recognize bacterial vitamin B metabolites presented by MR1. The document outlines that MAIT cells make up a significant percentage of T cells in the human body, particularly in the mucosa and liver. Their functions include roles in early detection of bacterial infection through cytokine production and cytotoxic activity. The document also notes that MAIT cells have been found infiltrating various human tumor tissues.
T cells recognize antigens through their T cell receptor, which is composed of two different chains and has one antigen-binding site. During T cell development in the thymus, gene rearrangement produces variability in the variable regions of the T cell receptor to recognize a wide range of antigens. When a T cell is stimulated by its antigen, there is no further mutation or switching of immunoglobulin constant region isotypes. T cell receptors function solely as antigen recognition molecules on the cell surface.
In vivo effects of Interleukin 2 on Lymphocyte Subpopulations in a Patient wi...Elke Stein
This document describes a clinical trial using interleukin-2 (IL-2) to treat a 17-month-old boy with combined immunodeficiency. IL-2 was purified from leukocytes and administered subcutaneously over 50 days. Within 3 weeks, IL-2 treatment normalized the patient's lymphocytosis and improved his eosinophilia. Most striking was the normalization of the patient's abnormal OKT4/OKT8 ratio and increase in OKT3+ cells. Infectious episodes decreased during treatment. Some effects were transient, returning to pathological levels after treatment ended.
This document outlines different types of regulatory T cells, including their identification, mechanisms of function, development processes, and properties. It discusses natural regulatory T cells that develop in the thymus and express high levels of CD25 and FoxP3, as well as induced regulatory T cells that develop in the periphery, including Tr1 cells that produce high levels of IL-10 and TGF-β, and Th3 cells that are induced following oral antigen administration and secrete TGF-β. The document also reviews CD8+ regulatory T cells and NKT regulatory cells, and compares the phenotypes, suppression mechanisms, targets, and roles of the different regulatory T cell subsets.
This document summarizes two scientific articles about Programmed Death-1 (PD-1) and its ligands PD-L1 and PD-L2. The first article analyzes the basal and induced expression of PD-1 ligands in three chordoma cell lines and finds that while basal expression is low, expression is upregulated by IFN-γ but not IL-4. The second article examines blocking the PD-1/PD-L1 pathway to prevent loss of effector function in adoptively transferred central memory CD8+ T cells against tumors.
The roles of the white blood cell subset γδ t cells within the human body are yet to be fully described.
Current literature has detailed several critical functions that vary dramatically between different γδ t cells.
Understanding how these elusive cells influence our immune systems will provide an opportunity to utilise their functions to assist medical treatments for a range of pathologies including cancer, diabetes, and bacterial infections.
Please send correspondence to Philip Voyias at P.D.Voyias@Warwick.ac.uk.
The document provides an overview of the immune system, including:
1) It describes the immune system as a complex, tiered system that distinguishes self from non-self via major histocompatibility complexes (MHCs) and recognizes antigens through both innate and adaptive responses.
2) The adaptive immune response involves an afferent limb for antigen recognition and presentation and an efferent limb that elicits effector responses through T cells, B cells, cytokines and antibodies.
3) Organ transplant rejection can occur via direct recognition of donor MHCs or indirect recognition of donor MHC fragments, with acute rejection being the most common type of allograft response.
Regulatory T cells (Tregs) play an important role in maintaining immune tolerance and suppressing excessive immune responses. Tregs can develop naturally in the thymus or be induced in the periphery. They express the transcription factor FoxP3 and surface markers CD4 and CD25. Tregs suppress the activation and functions of other immune cells and help prevent autoimmunity, control infections, allow transplantation tolerance, and support fetal-maternal tolerance in pregnancy. Dysregulation of Tregs has been linked to immunological diseases. Therapeutic use of Tregs may help treat diseases driven by excessive immune responses like autoimmunity.
This document provides an overview of mucosal-associated invariant T cells (MAIT). It discusses that MAIT cells are a type of innate alpha beta T cell that express a semi-invariant T cell receptor and recognize bacterial vitamin B metabolites presented by MR1. The document outlines that MAIT cells make up a significant percentage of T cells in the human body, particularly in the mucosa and liver. Their functions include roles in early detection of bacterial infection through cytokine production and cytotoxic activity. The document also notes that MAIT cells have been found infiltrating various human tumor tissues.
T cells recognize antigens through their T cell receptor, which is composed of two different chains and has one antigen-binding site. During T cell development in the thymus, gene rearrangement produces variability in the variable regions of the T cell receptor to recognize a wide range of antigens. When a T cell is stimulated by its antigen, there is no further mutation or switching of immunoglobulin constant region isotypes. T cell receptors function solely as antigen recognition molecules on the cell surface.
In vivo effects of Interleukin 2 on Lymphocyte Subpopulations in a Patient wi...Elke Stein
This document describes a clinical trial using interleukin-2 (IL-2) to treat a 17-month-old boy with combined immunodeficiency. IL-2 was purified from leukocytes and administered subcutaneously over 50 days. Within 3 weeks, IL-2 treatment normalized the patient's lymphocytosis and improved his eosinophilia. Most striking was the normalization of the patient's abnormal OKT4/OKT8 ratio and increase in OKT3+ cells. Infectious episodes decreased during treatment. Some effects were transient, returning to pathological levels after treatment ended.
This document outlines different types of regulatory T cells, including their identification, mechanisms of function, development processes, and properties. It discusses natural regulatory T cells that develop in the thymus and express high levels of CD25 and FoxP3, as well as induced regulatory T cells that develop in the periphery, including Tr1 cells that produce high levels of IL-10 and TGF-β, and Th3 cells that are induced following oral antigen administration and secrete TGF-β. The document also reviews CD8+ regulatory T cells and NKT regulatory cells, and compares the phenotypes, suppression mechanisms, targets, and roles of the different regulatory T cell subsets.
This document summarizes two scientific articles about Programmed Death-1 (PD-1) and its ligands PD-L1 and PD-L2. The first article analyzes the basal and induced expression of PD-1 ligands in three chordoma cell lines and finds that while basal expression is low, expression is upregulated by IFN-γ but not IL-4. The second article examines blocking the PD-1/PD-L1 pathway to prevent loss of effector function in adoptively transferred central memory CD8+ T cells against tumors.
Antigen specific T cell activation assay is one of the technologies we can provide during the one-stop service which can activate CAR-T cells for further downstream research or clinical trials. T cell activation requires at least two signals to be fully activated. The first signal is provided by the interaction of T cell antigen-specific receptor and the antigen-major histocompatibility complex (MHC).
https://www.creative-biolabs.com/car-t/antigen-specific-t-cell-activation-assay.htm
This document summarizes cell-mediated immunity. It discusses how T lymphocytes are responsible for cell-mediated immunity, with cytotoxic T cells destroying infected cells and helper T cells activating other immune cells through cytokine release. Antigens from intracellular pathogens are presented on MHC class I to cytotoxic T cells, while extracellular pathogens are presented on MHC class II to helper T cells. The document also describes T cell receptor structure and diversity, antigen recognition, and the mechanisms of cytotoxic T cell and helper T cell activation.
Mechanism of immune response ami and cmiPrasad Gunjal
The document discusses the mechanisms of immune response, specifically antibody-mediated immunity and cell-mediated immunity. It begins by defining immune response and dividing it into two types: humoral immune response and cell-mediated immune response. It then provides details on antigen presentation, helper T cell activation and differentiation, and the roles of the TH1 and TH2 cell subsets in directing antibody-mediated versus cell-mediated immunity. Key components of both response types are summarized, including the functions of cytokines produced.
This document summarizes T lymphocyte development and activation. It describes how progenitor cells commit to the T cell lineage in the bone marrow and thymus. In the thymus, T cells undergo proliferation, rearrangement of T cell receptor genes, and positive and negative selection. This results in functionally distinct T cell subsets that migrate to lymph nodes upon activation. T cell activation requires three signals - engagement of the T cell receptor by peptide-MHC complexes, costimulatory molecules such as CD28 binding to B7, and cytokine signals. This leads to intracellular signaling cascades and expression of genes regulating T cell effector function.
The document summarizes key aspects of major histocompatibility complex (MHC) molecules and T cell receptor (TCR) recognition. It discusses how MHC genes were found to be important in transplant rejection and immune responses. There are three classes of MHC molecules - Class I found on nucleated cells, Class II on antigen presenting cells, and Class III molecules like complement components. The TCR recognizes antigen peptides bound to MHC molecules. Both MHC and TCR are highly polymorphic and recognize antigens in a MHC-restricted manner.
Recognition of transplanted cells is determined by polymorphic MHC genes inherited from both parents. Alloantigen elicit cell-mediated and humoral immune responses from components like antigen presenting cells, B cells, antibodies, and T cells. Cytokines also mediate graft rejection. HLA matching and immunosuppressive drugs are used to minimize rejection, but chronic rejection remains a problem. New methods using genomic analysis and RNA sequencing are being developed to better determine HLA type for transplantation matching.
The document discusses disorders of immunity and the immune system. It provides information on key components of the immune system including antigens, antibodies, lymphocytes (T cells, B cells, NK cells), macrophages, dendritic cells, cytokines and the complement system. It also describes the major histocompatibility complex (MHC) and HLA antigens, noting that class I MHC antigens are expressed on all nucleated cells and present intracellular peptides to CD8 T cells, while class II MHC antigens are only expressed on antigen presenting cells and present extracellular peptides to CD4 T cells. HLA antigens play an important role in self-recognition and transplant rejection.
Cord blood is a potential source of natural killer (NK) cells for cancer immunotherapy. NK cells can be expanded from cord blood units to sufficient clinical scales for treatment. Expanded cord blood NK cells have been shown to be as cytotoxic against tumors as peripheral blood NK cells. They have demonstrated activity against multiple myeloma and chronic lymphocytic leukemia in preclinical studies. A phase I/II clinical trial is exploring the use of ex vivo expanded cord blood NK cells combined with chemotherapy and autologous stem cell transplant for multiple myeloma. Additional strategies are being investigated to enhance the anti-tumor activity of cord blood NK cells, such as using lenalidomide or engineering the cells to improve homing to the bone marrow micro
The document provides an overview of humoral immune responses, including B cell activation, antigen recognition, and antibody production. It discusses helper T cell-dependent antibody responses to protein antigens, outlining the key steps: initial activation and migration of B and T cells; antigen presentation; CD40L-CD40 interaction; extrafollicular B cell activation; the germinal center reaction involving follicular dendritic cells and follicular helper T cells; isotype switching; affinity maturation; plasma cell and memory B cell differentiation. The roles of cytokines, transcriptional regulators, and the SAP protein in T follicular helper cell generation and germinal center development are also summarized.
1. Regulatory T cells (Tregs) that express the transcription factor Foxp3 play a key role in controlling immune responses and maintaining immunological self-tolerance. Depletion of Tregs can lead to development of autoimmune diseases and inflammatory conditions.
2. Foxp3 is required for the development and function of Tregs. Mutations that inactivate Foxp3 result in fatal autoimmune diseases in both mice and humans. Depletion of Tregs through the removal of CD25+ cells or neutralization of IL-2 can also induce autoimmunity in normal animals.
3. Tregs constitutively express high levels of CD25 (the IL-2 receptor alpha chain) and depend on IL
Autoimmunity disorders occur when the immune system mounts an attack against the body's own tissues and organs. They are difficult to diagnose due to nonspecific initial symptoms, fluctuating symptoms, and the potential for multiple autoimmune conditions. Diagnostic methods include initial laboratory tests of inflammatory markers and autoantibodies, immunological studies, flow cytometry to analyze immune cells, cytokine studies, and examination of major histocompatibility complex genes associated with autoimmunity. A variety of autoantibodies against nuclear, cytoplasmic, and other cellular components can indicate autoimmune disease patterns and targets.
1) The document discusses humoral immunity and the mechanisms of antibody diversity. It describes how antibodies are produced through gene rearrangement of immunoglobulin genes, resulting in a huge variety of possible antibody structures.
2) Gene rearrangement of the heavy and light chain gene segments, along with junctional diversity and somatic hypermutation, allow for millions of different antibody combinations to be produced. This ensures antibodies can recognize a wide range of pathogens.
3) The key mechanisms that generate antibody diversity are combinatorial diversity through rearrangement of variable gene segments, junctional diversity through additions/deletions at gene junctions, and somatic hypermutation of rearranged genes in mature B cells.
The document summarizes key concepts in immunology related to cancer and organ transplants. It discusses how the immune system can recognize and respond to tumors, mechanisms by which tumors evade immune detection, and approaches to cancer immunotherapy. It also covers immune mechanisms of graft rejection, types of transplants, and strategies to prevent rejection through immunosuppression.
The document summarizes the immune system's responses to infectious diseases. It describes three levels of defense - epithelial barriers, innate immune responses, and acquired immune responses. The innate immune responses provide non-specific protection and include phagocytic cells, natural killer cells, complement proteins, acute-phase proteins, and cytokines. The acquired immune responses improve upon repeat exposure and involve antigen-specific B and T cells that work together to eliminate pathogens.
The document discusses genotyping and single nucleotide polymorphisms (SNPs). It explains that genotyping provides a measurement of genetic variation between species and describes the process of real-time polymerase chain reaction (PCR) used for genotyping. Several examples of SNPs are given, including ones related to obesity (SPP1), muscle function (ATP2A1), and apoptosis (MTCH2).
Humoral immunity is mediated by antibodies and functions to neutralize extracellular microbes and toxins. B-cells respond to and produce antibodies specific for many molecule types. When a B-cell encounters an antigen, it becomes activated and differentiates into a plasma cell that secretes antibodies of that specificity. T-cell help is required for effective antibody responses against protein antigens and drives affinity maturation and isotype switching.
The document discusses the evolution of adaptive immunity from innate immunity. It proposes that most adaptive immune molecules arose from innate molecules, with some exceptions like C3, MHC, and TdT. Adaptive molecules evolved abruptly, making it difficult to isolate their precursors. Some molecules evolved partly for immune functions while retaining other functions. B cell receptors, T cell receptors, RAG, TdT and parts of the complement system have identifiable innate precursors. MHC class II molecules evolved from molecules like DM that were involved in antigen processing. The adaptive immune system is unique to higher organisms and vertebrates.
The major histocompatibility complex (MHC) is a cluster of genes found in all mammals that encodes proteins important for the immune system to distinguish self from non-self. MHC molecules are expressed on the cell surface and present peptide antigens to T cells. There are three main classes of MHC genes - class I presents endogenous peptides to cytotoxic T cells, class II presents exogenous peptides to helper T cells, and class III encodes non-antigen presenting proteins involved in immunity. MHC molecules have binding sites that allow them to bind a variety of peptide antigens through anchor residues, helping the immune system recognize a diverse array of pathogens. Polymorphism of MHC alleles within populations helps provide protection against rapidly mutating pathogens.
The researchers identified 120 effector gene candidates from the wheat stem rust fungus Puccinia graminis f. sp. tritici (Pgt) using bioinformatics. They tested 65 of these candidates in rice using transient expression assays and identified 6 that were potentially recognized by rice resistance genes. Two Pgt effector genes are being further characterized as potential suppressors of plant cell death. The long term goals are to isolate Pgt effectors recognized by rice resistance genes, isolate the corresponding rice resistance genes, and transfer the rice resistance genes into wheat to develop rust resistance.
Start-Up Peru provides grants to innovative entrepreneurs in order to promote economic diversification and growth in Peru. It has funded 172 startups across 20 regions of Peru since launching four years ago, providing over 15.5 million soles in grants. The program evaluates proposals and assigns selected startups to business incubators who provide technical support and training. Start-Up Peru aims to support a new generation of businesses with greater added value that can differentiate, grow and expand over time.
COULD THE CHALLENGER ACCIDENT HAVE BEEN AVOIDEDAja Aj
The document analyzes the 1986 Challenger space shuttle accident that resulted in 7 deaths. It identifies problems with communication between technicians and management at NASA, as technicians warned of technical faults with the shuttle but management disregarded their concerns and felt pressure to launch from NASA. The document proposes developing proper communication channels between technicians and management, ensuring management listens to technicians' views without fear of reprisal, and having freedom of expression to prevent similar tragedies from occurring.
Antigen specific T cell activation assay is one of the technologies we can provide during the one-stop service which can activate CAR-T cells for further downstream research or clinical trials. T cell activation requires at least two signals to be fully activated. The first signal is provided by the interaction of T cell antigen-specific receptor and the antigen-major histocompatibility complex (MHC).
https://www.creative-biolabs.com/car-t/antigen-specific-t-cell-activation-assay.htm
This document summarizes cell-mediated immunity. It discusses how T lymphocytes are responsible for cell-mediated immunity, with cytotoxic T cells destroying infected cells and helper T cells activating other immune cells through cytokine release. Antigens from intracellular pathogens are presented on MHC class I to cytotoxic T cells, while extracellular pathogens are presented on MHC class II to helper T cells. The document also describes T cell receptor structure and diversity, antigen recognition, and the mechanisms of cytotoxic T cell and helper T cell activation.
Mechanism of immune response ami and cmiPrasad Gunjal
The document discusses the mechanisms of immune response, specifically antibody-mediated immunity and cell-mediated immunity. It begins by defining immune response and dividing it into two types: humoral immune response and cell-mediated immune response. It then provides details on antigen presentation, helper T cell activation and differentiation, and the roles of the TH1 and TH2 cell subsets in directing antibody-mediated versus cell-mediated immunity. Key components of both response types are summarized, including the functions of cytokines produced.
This document summarizes T lymphocyte development and activation. It describes how progenitor cells commit to the T cell lineage in the bone marrow and thymus. In the thymus, T cells undergo proliferation, rearrangement of T cell receptor genes, and positive and negative selection. This results in functionally distinct T cell subsets that migrate to lymph nodes upon activation. T cell activation requires three signals - engagement of the T cell receptor by peptide-MHC complexes, costimulatory molecules such as CD28 binding to B7, and cytokine signals. This leads to intracellular signaling cascades and expression of genes regulating T cell effector function.
The document summarizes key aspects of major histocompatibility complex (MHC) molecules and T cell receptor (TCR) recognition. It discusses how MHC genes were found to be important in transplant rejection and immune responses. There are three classes of MHC molecules - Class I found on nucleated cells, Class II on antigen presenting cells, and Class III molecules like complement components. The TCR recognizes antigen peptides bound to MHC molecules. Both MHC and TCR are highly polymorphic and recognize antigens in a MHC-restricted manner.
Recognition of transplanted cells is determined by polymorphic MHC genes inherited from both parents. Alloantigen elicit cell-mediated and humoral immune responses from components like antigen presenting cells, B cells, antibodies, and T cells. Cytokines also mediate graft rejection. HLA matching and immunosuppressive drugs are used to minimize rejection, but chronic rejection remains a problem. New methods using genomic analysis and RNA sequencing are being developed to better determine HLA type for transplantation matching.
The document discusses disorders of immunity and the immune system. It provides information on key components of the immune system including antigens, antibodies, lymphocytes (T cells, B cells, NK cells), macrophages, dendritic cells, cytokines and the complement system. It also describes the major histocompatibility complex (MHC) and HLA antigens, noting that class I MHC antigens are expressed on all nucleated cells and present intracellular peptides to CD8 T cells, while class II MHC antigens are only expressed on antigen presenting cells and present extracellular peptides to CD4 T cells. HLA antigens play an important role in self-recognition and transplant rejection.
Cord blood is a potential source of natural killer (NK) cells for cancer immunotherapy. NK cells can be expanded from cord blood units to sufficient clinical scales for treatment. Expanded cord blood NK cells have been shown to be as cytotoxic against tumors as peripheral blood NK cells. They have demonstrated activity against multiple myeloma and chronic lymphocytic leukemia in preclinical studies. A phase I/II clinical trial is exploring the use of ex vivo expanded cord blood NK cells combined with chemotherapy and autologous stem cell transplant for multiple myeloma. Additional strategies are being investigated to enhance the anti-tumor activity of cord blood NK cells, such as using lenalidomide or engineering the cells to improve homing to the bone marrow micro
The document provides an overview of humoral immune responses, including B cell activation, antigen recognition, and antibody production. It discusses helper T cell-dependent antibody responses to protein antigens, outlining the key steps: initial activation and migration of B and T cells; antigen presentation; CD40L-CD40 interaction; extrafollicular B cell activation; the germinal center reaction involving follicular dendritic cells and follicular helper T cells; isotype switching; affinity maturation; plasma cell and memory B cell differentiation. The roles of cytokines, transcriptional regulators, and the SAP protein in T follicular helper cell generation and germinal center development are also summarized.
1. Regulatory T cells (Tregs) that express the transcription factor Foxp3 play a key role in controlling immune responses and maintaining immunological self-tolerance. Depletion of Tregs can lead to development of autoimmune diseases and inflammatory conditions.
2. Foxp3 is required for the development and function of Tregs. Mutations that inactivate Foxp3 result in fatal autoimmune diseases in both mice and humans. Depletion of Tregs through the removal of CD25+ cells or neutralization of IL-2 can also induce autoimmunity in normal animals.
3. Tregs constitutively express high levels of CD25 (the IL-2 receptor alpha chain) and depend on IL
Autoimmunity disorders occur when the immune system mounts an attack against the body's own tissues and organs. They are difficult to diagnose due to nonspecific initial symptoms, fluctuating symptoms, and the potential for multiple autoimmune conditions. Diagnostic methods include initial laboratory tests of inflammatory markers and autoantibodies, immunological studies, flow cytometry to analyze immune cells, cytokine studies, and examination of major histocompatibility complex genes associated with autoimmunity. A variety of autoantibodies against nuclear, cytoplasmic, and other cellular components can indicate autoimmune disease patterns and targets.
1) The document discusses humoral immunity and the mechanisms of antibody diversity. It describes how antibodies are produced through gene rearrangement of immunoglobulin genes, resulting in a huge variety of possible antibody structures.
2) Gene rearrangement of the heavy and light chain gene segments, along with junctional diversity and somatic hypermutation, allow for millions of different antibody combinations to be produced. This ensures antibodies can recognize a wide range of pathogens.
3) The key mechanisms that generate antibody diversity are combinatorial diversity through rearrangement of variable gene segments, junctional diversity through additions/deletions at gene junctions, and somatic hypermutation of rearranged genes in mature B cells.
The document summarizes key concepts in immunology related to cancer and organ transplants. It discusses how the immune system can recognize and respond to tumors, mechanisms by which tumors evade immune detection, and approaches to cancer immunotherapy. It also covers immune mechanisms of graft rejection, types of transplants, and strategies to prevent rejection through immunosuppression.
The document summarizes the immune system's responses to infectious diseases. It describes three levels of defense - epithelial barriers, innate immune responses, and acquired immune responses. The innate immune responses provide non-specific protection and include phagocytic cells, natural killer cells, complement proteins, acute-phase proteins, and cytokines. The acquired immune responses improve upon repeat exposure and involve antigen-specific B and T cells that work together to eliminate pathogens.
The document discusses genotyping and single nucleotide polymorphisms (SNPs). It explains that genotyping provides a measurement of genetic variation between species and describes the process of real-time polymerase chain reaction (PCR) used for genotyping. Several examples of SNPs are given, including ones related to obesity (SPP1), muscle function (ATP2A1), and apoptosis (MTCH2).
Humoral immunity is mediated by antibodies and functions to neutralize extracellular microbes and toxins. B-cells respond to and produce antibodies specific for many molecule types. When a B-cell encounters an antigen, it becomes activated and differentiates into a plasma cell that secretes antibodies of that specificity. T-cell help is required for effective antibody responses against protein antigens and drives affinity maturation and isotype switching.
The document discusses the evolution of adaptive immunity from innate immunity. It proposes that most adaptive immune molecules arose from innate molecules, with some exceptions like C3, MHC, and TdT. Adaptive molecules evolved abruptly, making it difficult to isolate their precursors. Some molecules evolved partly for immune functions while retaining other functions. B cell receptors, T cell receptors, RAG, TdT and parts of the complement system have identifiable innate precursors. MHC class II molecules evolved from molecules like DM that were involved in antigen processing. The adaptive immune system is unique to higher organisms and vertebrates.
The major histocompatibility complex (MHC) is a cluster of genes found in all mammals that encodes proteins important for the immune system to distinguish self from non-self. MHC molecules are expressed on the cell surface and present peptide antigens to T cells. There are three main classes of MHC genes - class I presents endogenous peptides to cytotoxic T cells, class II presents exogenous peptides to helper T cells, and class III encodes non-antigen presenting proteins involved in immunity. MHC molecules have binding sites that allow them to bind a variety of peptide antigens through anchor residues, helping the immune system recognize a diverse array of pathogens. Polymorphism of MHC alleles within populations helps provide protection against rapidly mutating pathogens.
The researchers identified 120 effector gene candidates from the wheat stem rust fungus Puccinia graminis f. sp. tritici (Pgt) using bioinformatics. They tested 65 of these candidates in rice using transient expression assays and identified 6 that were potentially recognized by rice resistance genes. Two Pgt effector genes are being further characterized as potential suppressors of plant cell death. The long term goals are to isolate Pgt effectors recognized by rice resistance genes, isolate the corresponding rice resistance genes, and transfer the rice resistance genes into wheat to develop rust resistance.
Start-Up Peru provides grants to innovative entrepreneurs in order to promote economic diversification and growth in Peru. It has funded 172 startups across 20 regions of Peru since launching four years ago, providing over 15.5 million soles in grants. The program evaluates proposals and assigns selected startups to business incubators who provide technical support and training. Start-Up Peru aims to support a new generation of businesses with greater added value that can differentiate, grow and expand over time.
COULD THE CHALLENGER ACCIDENT HAVE BEEN AVOIDEDAja Aj
The document analyzes the 1986 Challenger space shuttle accident that resulted in 7 deaths. It identifies problems with communication between technicians and management at NASA, as technicians warned of technical faults with the shuttle but management disregarded their concerns and felt pressure to launch from NASA. The document proposes developing proper communication channels between technicians and management, ensuring management listens to technicians' views without fear of reprisal, and having freedom of expression to prevent similar tragedies from occurring.
A service product comprises tangible and intangible elements that create value for customers. The core product is accompanied by supplementary services that facilitate and enhance the customer experience. Together, the core product and supplementary services make up the service concept. Marketers must identify all elements of the service and decide which to include as part of the overall offering.
This document provides a lesson plan on parts of the body for children. The aims are to present and talk about parts of the body while pointing to them. Key vocabulary includes head, eyes, nose, mouth, ears, and legs. The warm up has students look at a picture and count balls. They will then look at another picture and answer questions by identifying parts like "this is a nose". Finally, students do actions like touching their head, eyes, nose, ears, mouth, and legs while looking at a body picture.
This document provides a lesson plan on parts of the body for children. The aims are to present and talk about parts of the body while pointing to them. Key vocabulary includes head, eyes, nose, mouth, ears, and legs. The warm up has students look at a picture and count balls. They will then look at another picture and answer questions by identifying parts like "this is a nose". Finally, students do actions like touching their head, eyes, nose, ears, mouth, legs, and face.
The document discusses new product development and a product's life cycle. It describes the typical stages in new product development as idea generation, screening, concept development and testing, marketing strategy development, business analysis, product development, test marketing, and commercialization. It also outlines the stages in a product's life cycle as development, introduction, growth, maturity, and decline. The document provides strategies for marketing a product through each stage of its life cycle.
The Australian Residential Property Market & Economy: Quarterly Review, May 2015
Take a look at a comprehensive Australian housing market overview put together by CoreLogic RP Data.
State-wide residential property sales in Queensland reached a five-year high in 2014. Southeast Queensland, Toowoomba, and Cairns performed strongly, while most regional centers lagged behind due to factors like the downturn in mining and drought. House prices increased across southeast Queensland in 2014 compared to the previous year. The improving conditions in southeast Queensland are expected to boost the state's real estate market in the coming year.
Can you change multinationals strategies with social media?SocialMedia Summit
Greenpeace is a NGO striving to protect the environment. To do so, they use every kind of creative, non-violent action, including an intensive communication through social media. Dave will share Greenpeace’s strategy on how to use social media to help and achieve its environmental objectives.
Dave Van Meel, Head of Communications, Greenpeace
The document discusses the evolution of buyer-supplier relationships from reactive transactions to strategic partnerships. It describes three types of relationships - transactional, collaborative, and alliance. Transactional relationships focus on price and are short-term, while collaborative and alliance relationships aim for lower total costs and improved performance through open communication, long-term contracts, and shared goals. Alliances require the highest levels of trust and commitment between partners to fully realize benefits like reduced costs, improved quality, and faster innovation.
The document discusses a course on decision making skills that aims to build analytical abilities, capabilities for decision making, and understanding of issues affecting organizations. The main teaching method is case studies, which present real-life business problems. Students must integrate knowledge from various business functions to analyze cases and recommend solutions. A sample case involves a hotel deciding whether to accept a promotional offer from a cricket event management team involving discounted rooms. While the hotel has spare capacity, accepting would result in lost revenue and dissatisfied regular customers. For marketing, financial, and HR reasons, the management should refuse the deal.
This document provides an introduction to business ethics. It defines business ethics as the study of business situations, activities, and decisions where issues of right and wrong are addressed. It distinguishes business ethics from morality and the law. Morality refers to norms and values that define right and wrong, ethics is the study and rationalization of morality through reasoned principles and theories, and the law establishes minimum acceptable standards of behavior. The document outlines some of the debates around business ethics and discusses the importance of studying ethics in business decision-making.
SEO involves optimizing websites to increase their visibility in search engine results. Key factors include choosing relevant keywords, optimizing page titles and descriptions with those keywords, and following technical guidelines like using hyphens in file names, submitting sitemaps to search engines, and ensuring pages load quickly across browsers. Search engines use crawler programs called spiders to index websites by reading HTML source code and following links, with the robots.txt file guiding spiders on what to index or avoid.
The numbers of house sales across Queensland peaked in the last quarter of 2013, with nearly 10,000 sales. This was the highest quarterly sales volume in several years and occurred without stimulus measures. The improving housing market and growing consumer confidence contributed to the increased sales. Median house prices also increased over the quarter in most regions of Queensland, with Brisbane prices up 6%, reflecting a jump in sales of properties between $500,000-$1 million.
The document outlines the typical structure and contents of a research report, including 5 chapters. Chapter 1 introduces the topic and conceptual framework. Chapter 2 reviews relevant literature, provides the rationale and objectives of the study. Chapter 3 describes the research methodology, including the design, data collection tools, and analysis methods. Chapter 4 presents and discusses the results. Chapter 5 states the conclusions, implications, limitations, and scope for future work. The document then provides examples of the contents of Chapters 1-3 for a research report on analyzing the financial performance of Sintex Industries Ltd. over the last 3 years. It discusses the company background, products, achievements and financial analysis methods like ratio analysis.
This document discusses immunity and hypersensitivity. It defines key terms like allergen, allergy, allogeneic, allograft, atopy, and more. It also describes different immune cells like B lymphocytes, T lymphocytes, macrophages, and their roles. It discusses the major histocompatibility complex and its importance in transplantation and regulating immunity. Finally, it covers different diseases of immunity like immunodeficiencies, hypersensitivity reactions, autoimmune diseases, and acquired immunodeficiency syndrome (AIDS).
Innate immunity is the body's first line of defense against pathogens. It includes physical and chemical barriers like skin and stomach acid, immune cells like macrophages and neutrophils, and soluble proteins of the complement system. Innate immunity responds rapidly in a non-specific manner through pattern recognition receptors on cells that recognize conserved molecular patterns on pathogens. It has no immunological memory but helps initiate and regulate the adaptive immune response.
The document summarizes key aspects of the immune system. It discusses the central and peripheral organs of the immune system including the thymus, bone marrow, spleen, lymph nodes, and tonsils. It describes the development and maturation of white blood cells and B and T lymphocytes. It also summarizes the differences between humoral and cell-mediated immunity and the roles of B cells, T cells, antibodies, and cytokines in the immune response.
This document summarizes tools and techniques for studying the innate immune system. It describes the differences between innate and adaptive immunity, the phases and cellular components of the innate response, pattern recognition receptors, signaling pathways, and technologies for research including PCR arrays and reporter assays. An example is given of using a PCR array to study the role of TLR3 in the response to Chlamydia infection, finding that TLR3 and IFN-β are major mediators. Another example shows using a reporter array to identify NF-κB and other pathways activated by cytokine stimulation.
The document provides an overview of the immune system, including its normal functions, divisions, components, cells, molecules, and regulation. The key points are:
- The immune system protects against pathogens and prevents reinfection through immunological memory. Its divisions are the innate and adaptive systems.
- The innate system provides first response via nonspecific defenses like skin, phagocytes, and natural killer cells. The adaptive system responds antigen-specifically via T and B cells.
- T cells recognize antigen via T cell receptors and MHC molecules and mediate cellular immunity. B cells recognize antigen directly and produce antibodies for humoral immunity.
- Cytokines mediate communication between immune cells, directing immune responses. Regulatory
The document discusses various aspects of immunity including:
1. There are two types of immune responses - the primary response which is slower and involves IgM, and the secondary response which is faster and involves IgG.
2. Humoral immunity involves antibodies defending against extracellular pathogens and participating in hypersensitivity reactions.
3. The cellular immune response involves antigen processing, T cell activation, cytotoxic T cells attacking infected cells. Helper T cells activate other immune cells.
4. Autoimmunity occurs when the immune system mistakenly attacks self-antigens, leading to diseases like rheumatoid arthritis and diabetes. Immunodeficiency diseases impair the immune system's ability to function properly.
The document provides information on basic immunology concepts. It discusses the two means of acquiring immunity: active immunity where an individual makes their own antibodies after encountering an antigen, and passive immunity where preformed antibodies are transferred. It also describes the two main types of immune responses: the innate immune response individuals are born with, and the adaptive/acquired response that develops with exposure over time involving antibodies and T cells. Key cells of the immune system involved in these responses are also outlined, including lymphocytes, phagocytes, and the roles of cellular and humoral immunity.
This document summarizes cell-mediated immunity. It discusses that adaptive immunity has two effector mechanisms: humoral immunity mediated by antibodies, and cellular immunity mediated by cells that detect and eliminate intracellular pathogens. Cell-mediated immunity is carried out by cytotoxic T cells, helper T cells, natural killer cells, macrophages, and neutrophils. The activation of naive T cells requires interaction with antigen-presenting cells and co-stimulatory signals. Effector T cells secrete cytokines and express surface molecules that activate macrophages and induce target cell death. T regulatory cells also play an important role in regulating immune responses.
This document summarizes cell-mediated immunity. It discusses that adaptive immunity has two effector mechanisms: humoral immunity mediated by antibodies, and cellular immunity mediated by cells that detect and eliminate intracellular pathogens. Cell-mediated immunity is carried out by cytotoxic T cells, helper T cells, natural killer cells, macrophages, and neutrophils. The activation of naive T cells requires interaction with antigen-presenting cells and co-stimulatory signals. Effector T cells secrete cytokines and express surface molecules that activate macrophages and induce target cell death. T regulatory cells also play an important role in regulating immune responses.
Cell-mediated immunity involves the detection and elimination of intracellular pathogens and tumor cells by cells of the immune system. It is mediated by T cells, including CD8+ cytotoxic T cells and CD4+ T helper cells. CD8+ T cells directly kill infected cells through release of perforins and granzymes, while CD4+ T cells secrete cytokines that activate macrophages and other immune cells. Natural killer cells and macrophages also contribute to cell-mediated immunity through non-specific cytotoxic mechanisms. The activation and differentiation of T cells requires recognition of antigen presented by MHC molecules on antigen-presenting cells as well as co-stimulatory signals. Cytokines further regulate the development of T cell subsets such as Th1 and Th
This document summarizes various inflammatory mediators including cytokines, chemokines, lipid mediators, and neuropeptides. It describes the sources and functions of different cytokines such as IL-1, TNF-α, IFN-γ, and chemokines such as IL-8 and RANTES. It also discusses the roles of lipid mediators like leukotrienes and prostaglandins in inflammation.
The document discusses neuroimmunology and provides information on the immune system and its normal functions and disorders. It describes the innate and adaptive immune systems, including skin, phagocytes, natural killer cells, the complement system, antibodies, B cells, antigen presenting cells, major histocompatibility complex, toll-like receptors, T lymphocytes, cluster of differentiation markers, cytokines, chemokines, initiation and regulation of the immune response, termination of the immune response, self-tolerance, central tolerance, peripheral tolerance, anergy, regulatory T cells, immune privilege in the central nervous system, and several immune-mediated disorders of the nervous system including multiple sclerosis, myasthenia gravis, Guillain-Barré syndrome
This document discusses T-cell epitope vaccine design through immunoinformatics. It first defines immunoinformatics as the computational study of the immune response. It then discusses types of vaccines and properties of epitopes, focusing on T-cell epitopes which are recognized by T-cells. The document explains how vaccines provide protection by stimulating memory B and T cells to quickly respond when a pathogen is encountered. It also discusses reverse vaccinology and methods for predicting epitopes, including analyzing binding affinity to MHC molecules using structure-based or sequence-based methods.
This document provides an overview of the cells of the immune response. It describes the origin of immune cells from stem cells in the bone marrow and thymus. The main cells discussed are lymphocytes, including T cells which develop in the thymus and have T cell receptors, and B cells which develop in the bone marrow and have antibody receptors. The roles and subsets of T cells such as helper T cells, cytotoxic T cells, regulatory T cells, and memory T cells are summarized. The maturation and antigen-dependent selection of B cells into plasma cells that secrete antibodies is also outlined.
cellular and humoral components of immune System.vinu.pptxGokulVV3
This document summarizes the cellular and humoral components of the immune system. It discusses the primary and secondary lymphoid organs where immune cells develop and interact with antigens. The key immune cells discussed are T cells, B cells, natural killer cells, macrophages, and phagocytes. T cells recognize antigens through T cell receptors and can be helper, cytotoxic or memory cells. B cells mature in the bone marrow and produce antibodies when activated. The humoral and cellular immune responses mediated by B and T cells respectively provide adaptive immunity against pathogens.
1. The document presents information about T cells and B cells, including their development, activation, and functions.
2. T cells develop in the thymus gland and have roles in direct killing of infected cells and regulating the immune response. B cells mature in the bone marrow and produce antibodies to help fight pathogens.
3. Activation of both T and B cells involves interaction with antigen-presenting cells and costimulatory signals, leading to cell proliferation and differentiation into effector and memory cells.
A brief covering basics of immunity understanding and also allowing students to understand with ease the concepts of innate immunity, adaptive immunity, Tcell, Bcell, MHC molecular genetics, and also cytokines and also its role in various disease.
T CELL ACTIVATION AND IT'S TERMINATIONpremvarma064
T cell activation requires two signals: 1) recognition of antigens displayed on antigen-presenting cells by T cell receptors and 2) co-stimulatory signals through molecules like CD28. This leads T cells to proliferate, differentiate into effector and memory cells, and perform effector functions. Proper activation requires interaction between T cells and antigen-presenting cells in lymphoid tissues, where costimulatory molecules are highly expressed. Dysregulation of T cell activation can lead to autoimmunity or susceptibility to infection.
introduction of adaptive immunity. classification of adaptive immunity, factor affecting it and mechanism of adaptive immunity comparison between adaptive immunity and innate immunity. characteristic of adaptive immunity . cell mediated immune responses immunoglobulins
types of immunoglobulins. functions of immunoglobulins, hypersensitivity reactions
Fifth Annual Mitchell Memorial Lecture, October 6, 2014, at UC San Diego, featuring Dr. Jonathan Karn of Case Western Reserve University speaking on "Lessons Learned from models for HIV latency helping to formulate virus eradication strategies."
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1. Introduction to Immunology<br />1.1 General Properties of Immune Responses<br />1.1.1 Overview of immune responses in vivo<br />1.1.2 Classification<br />1.1.2.1 innate and adaptive immunity<br />Innate immunity<br />adaptive immunity<br />features<br />phases<br />1.1.2.2 humoral and cell-mediated immunity<br />humoral immunity<br />cell-mediated immunity<br />1.1.2.3 active and passive immunity<br />1.2 Components of Immune Systems<br />1.2.1 Tissues and organs of immune systems<br />1.2.1.1 generative organs (primary lymphoid organs)<br />Bone Marrow<br />Thymus<br />1.2.1.2 peripheral organs (secondary lymphoid organs)<br />lymph nodes<br />spleen<br />cutaneous immune system<br />mucosal immune system<br />1.2.2 Cells of immune systems<br />1.2.2.1 lymphoid progenitor cells <br />B lymphocytes<br />T lymphocytes<br />NK cells<br />NKT cells<br />1.2.2.2 myeloid progenitor cells<br />Granulocytes<br />Mast cells<br />Macrophages(Mononuclear phagocytes )<br />1.2.2.3 Dendritic cells(DC)<br />2. Recognition of Antigens<br />2.1 Innate immune cells and anitgen recognition<br />2.1.1 Pathogen associated molecular patterns(PAMPs)<br />2.1.2 Pattern recognition recptors(PRRs) and signaling pathways<br />2.1.2.1 PPRs<br />Membrane-bound PPRs<br />mannose receptor<br />Scavenger receptor<br />Toll-like receptor(TLR)<br />Cytoplasmic PRRs<br />NOD Like Receptors<br />RIG-I-like RNA helicase(RLH)<br />2.1.2.2 PRR(TLR/RLH) signalling pathway<br />TLR signaling pathway<br />Adaptor molecules in the pathway<br />two basic pathways<br />RLH signaling pathway<br />2.1.3 PAMPs and PRRs interations during viral infections<br />2.1.3.1 TLR/RLH recognition of viral infection<br />Vial recognition by TLRs<br />Viral recognition by RLHs<br />2.1.3.2 Viral antagonist of PRR signalling pathways<br />2.1.3.3 The therapeutic application of manipulation of PRR signalling pathways<br />2.2 T Lymphocytes and Antigen Recognition<br />2.2.1 The Major Histocompatibility Complex (MHC molecules)<br />2.2.1.1 Discovery of MHC<br />2.2.1.2 MHC genes<br />Properties of MHC genes<br />Genomic organiztion of MHC<br />Expression and regualtion of MHC genes<br />2.2.1.3 MHC molecules<br />Properties of MHC molecules<br />Structure of MHC molecules<br />2.2.1.4 MHC and peptide interations<br />Properties of MHC and peptide interations<br />Structures of MHC-peptide complex<br />Class I MHC<br />Class II MHC<br />Immune functions of MHC and peptide interations<br />2.2.2 Antigen Processing and Presentation to T Lymphocytes<br />2.2.2.1 Antigen presenting cells(APCs)<br />Professional APCs<br />Dendritic cells<br />Macrophages<br />B lymphocytes<br />non-professional APCs<br />2.2.2.2 Process of antigen presentation<br />Rout of antigen entry, capture and presentation in vivo<br />Antigen capture by APC and present to CD4 Th cells<br />Antigen presentation to CD8 T cells<br />Cellular pathways of protein antigen processing and presentation<br />MHC II-CD4 Th pathway<br />antigen uptake<br />antigen processing<br />MHC II synthesis and antigen loading<br />surface expression<br />MHC I- CD8 CTL pathway<br />antigen uptake<br />antigen processing<br />MHC I synthesis antigen loading<br />surface expression<br />Presentation of non-peptide antigens<br />2.2.3 T-cell receptor(TCR) and Accessory Molecules<br />2.2.3.1 T-cell receptor(TCR) complex (recognition and signaling)<br />TCR (αβ /γδ)<br />αβ TCR<br />γδ TCR<br />Signaling molecules<br />CD3<br />ζ chain<br />2.2.3.2 T-cell Accessory Molecules (adhesion and signaling)<br />Co-receptors:CD4 and CD8<br />structure<br />function<br />Co-stimulator:CD28 and CTLA-4<br />Signalling molecules:CD45 and CD2<br />adhesion molecules:integrins,selectins and CD44<br />2.2.3.3 Other molecules<br />cell markers<br />effector molecules<br />2.3 B Lymphocytes and Antigen Recognition<br />2.3.1 B-cell receptor(BCR) and Accessory Molecules<br />2.3.1.1 Structure and roles<br />2.3.1.2 BCR complex vs TCR complex<br />2.3.2 Antibodies<br />2.3.2.1 Ig structure<br />Chains<br />Ig domains<br />Various region<br />Constant region<br />Hinge region<br />2.3.2.2 Ig classification(Isotypes)<br />2.3.2.3 Ig synthesis<br />General process<br />B cell maturation and Ig modification<br />2.3.2.4 Ig function<br />2.3.3 Antibodies(Ab) and antigen recognition<br />2.3.3.1 Antigens(Ag)<br />Epitope and Ag determinant<br />Antigenicity and immunogenicity<br />Properties of the immunogen contribute to immunogenicity<br />Properties of the immunogen<br />Foreignness<br />Molecular Size<br />Chemical Composition and Heterogeneity<br />Susceptibility to Antigen Processing and Presentation<br />Biological system<br />Genotype of the Recipient Animal<br />Immunogen Dosage and Route of Administration<br />Adjuvant<br />2.3.3.2 Antigen recognition<br />Three antigen-recognizing molecules<br />Immunoglobulin(Ig)<br />T cell receptor(TCR)<br />The Major Histocompatibility Complex (MHC molecules)<br />others<br />B cell recognition of Antigens<br />Characteristic properties of B-cell epitopes<br />Properties of antigen and antibody reaction<br />Different antibodies<br />Polyclonal Abs & Monoclonal Abs<br />Anti-Ig Antibodies<br />3. Maturation of B&T lymphocytes<br />3.1 General features of both T and B Lymphocyte maturation<br />3.1.1 Stages of lymphocytes maturation<br />3.1.1.1 Early maturation(produce cell pools)<br />3.1.1.2 Gene recombination(produce antigen receptor repertoires)<br />3.1.1.3 Late maturation(selection of antigen receptor repertoires)<br />3.1.1.4 Functional maturation(produce surface and intracellular effector molecules )<br />3.1.2 Diversity of antigen receptors(BCR/Ig and TCR) <br />3.1.2.1 Germline organiztion of antigen receptor genes<br />3.1.2.2 Different levels of the generation of diversity<br />3.1.2.3 Mechanisms of the generation of diversity<br />DNA re-arrange(somatic recombination): DNA combinational diversity<br />Type of recombination<br />Mechanism of recombination<br />DNA modification: DNA junctional diversity<br />RNA alternative splicing of constant region<br />3.2 B lymphocytes maturation<br />3.2.1 Stages of B lymphocytes maturation<br />3.2.1.1 Pro-B cell<br />3.2.1.2 Pre-B cell<br />3.2.1.3 Immature B cell<br />3.2.1.4 Mature B cell<br />3.2.2 Types of B cells<br />3.3 T lymphocytes maturation<br />3.3.1 Stages of T lymphocytes maturation<br />3.3.1.1 Pro-T cell<br />3.3.1.2 Early Pre-T cell(double negative)<br />3.3.1.3 Late Pre-T cell(double positive)<br />3.3.1.4 Immature T cell(single positive)<br />3.3.1.5 Mature T cell<br />3.3.2 gd-TCR subset of T lymphocytes<br />4. Activation and Regulation of Lymphocytes (Respond to Antigens)<br />4.1 Activation of T Lymphocytes<br />4.1.1 Biological process (immune responses)<br />4.1.1.1 Initial activation<br />receptor(TCR) and coreceptor(CD4 and CD-8): recognition of antigen(1st signal)<br />costimulators(2nd signal)<br />4.1.1.2 Immune responses<br />cytokines secretion<br />proliferation<br />differentiation<br />4.1.2 Biochemical mechanism (signal transduction)<br />4.1.2.1 Signal reception (across membrane)<br />triggering<br />clustering<br />signal initiation<br />4.1.2.2 Signal amplification (pathway in the cell)<br />Ras-MAP kianse pathway<br />PLCg-mediated pathways<br />4.1.2.3 Signal destination<br />4.1.3 Signal pathways of T cell activation in the whole map <br />4.1.3.1 Signaling molecules<br />signal receptors<br />Channel-linked receptor<br />G-protein-linked receptor<br />Enzyme linked receptor<br />Non-enzyme linked receptor<br />non-receptor signaling molecules<br />membrane protein<br />receptor associated membrane proteins<br />membrane associate protein<br />non-membrane proteins<br />4.1.3.2 Signaling pathways<br />signal reception<br />passive difussion<br />iron channel<br />G-protein linked signaling transduction system<br />enzyme-linked signal transduction system<br />PTK receptor<br />PTK associated recptor<br />CD4/CD8<br />Try phosphatase receptor<br />Ser/Thr kinase receptor<br />Guanine cyclase receptor<br />signal amplification<br />cascade enzyme amplification<br />second signal linked enzyme amplification<br />directly enter nucleus<br />signal destination<br />effector enzyme<br />gene expression by transcription factor<br />4.2 Activation of B Lymphocytes<br />4.2.1 Biological process (immune responses)<br />4.2.1.1 Activation by T cell dependent antigens(protein antigen; TD antigen)<br />Initial activation by TD antigens(T cell dependent antigen)<br />Activation by helper T cell (T:B cell interation)<br />antigen-induced migration of B and helper T cells<br />presentation of protein antigens by B cell to helper T cells<br />Helper T cell-Mediated activation of B cells<br />Immune responses (proliferation and differentiation)<br />immune responses induced by TD antigen activation.<br />immune responses induced by helper T activation<br />Early events<br />B cell proliferation<br />antibody secretion (from membrane Ig to secreting Ig)<br />isotype switching<br />Late events<br />affinity maturation<br />Memory B cells<br />Primary vs. secondary humoral immune response<br />4.2.1.2 Activation by T cell independent antigen (nonprotein antigen;TI antigen)<br />Activation by TI antigen<br />Immune responses induced by IT antigen<br />4.2.1.3 Role of complement in B cell activation<br />4.2.1.4 Factors that influence the amount and type of Ab produced<br />4.2.2 Biological mechanism (signal transduction)<br />4.2.2.1 signal reception(across membrane)<br />triggering of activation<br />initiation of activation<br />4.2.2.2 signal amplification(pathway in the cell)<br />4.2.2.3 signal destination<br />4.2.3 Antibody responses and feedback<br />5. Effector mechanism of Immune Response (Eliminate Antigens)<br />5.1 Effector function of innate immunity<br />5.1.1 Epithelial barriers<br />5.1.2 Innate immune cells<br />5.1.2.1 Phagocytes<br />Neutrophiles <br />Macrophage<br />5.1.2.2 Dendric cells<br />5.1.2.3 NK cells<br />Overview<br />recognition and activation<br />effector functions<br />NK Cell Phenotype and Distribution<br />NK cell recognition of its target cells<br />NK Cell Receptors<br />Classification<br />By specificity<br />Summary of MHC I specific receptors:<br />Summary of MHC I non-specific receptors<br />Related T cell receptors<br />By structure and function<br />Functional subsets of natural killer cells<br />Functions<br />Missing Self Hypothesis<br />Integration of Stimulatory and Inhibitory Signaling<br />Adhesion molecules in formation of NK cell–target cell conjugates<br />The immunoreceptor tyrosine-based activation motif-dependent activation pathways<br />The DAP10-dependent, ITAM-independent activation pathway<br />Natural Killer Cell Differentiation<br />Role of NK cells in diseases <br />Viral Infections<br />Intracellular Microbes<br />Cancer<br />5.1.3 Effector proteins<br />5.1.3.1 Anti-microbial peptides<br />5.1.3.2 Acute phase response proteins (APR proteins)<br />Complement system<br />Features of complement system<br />Pathways of complement activation<br />classical pathway(activated by antibody)<br />alternative pathway<br />lectin pathway<br />Effector function of complement activation<br />complement-mediated cytolysis<br />comlement mediated opsonization and phagocytosis<br />stimulation of inflammatory responses<br />other functions<br />Regulation of complement activation<br />regulators of complement activation<br />mechanisms of regulation <br />other APR proteins<br />5.2 Effector function of adaptive immunity<br />5.2.1 Effector function of Cell-mediated immunity(CMI)<br />5.2.1.1 Types of cell-mediated immunity<br />Effector function of NK cells<br />Effector function CD4 Th1 cells<br />Effector functions of CD4 Th2 cells<br />Effector function of CD8 CTL<br />Effector CTLs Are Generated from CTL Precursors<br />Two CTL killing mechanisms<br />5.2.1.2 General properties of effector T cells<br />The Activation Requirements of T Cells Differ<br />Cell-Adhesion Molecules Facilitate TCR-Mediated Interactions<br />Effector T Cells Express a Variety of Effector Molecules<br />5.2.1.3 Phases of Cell-mediated immune responses<br />Development of effector T cells in peripheral lymphoid organs<br />antigen recognition and activation<br />clonal expansion<br />differentiation<br />naive CD4 cells to Subsets of effector cells<br />Naive CD8 cells to CTLs<br />Migration and retention of leukocytes to infection sites<br />Effector mechanism of cell-mediated immunity<br />5.2.2 Effector function of Humoral immunity<br />5.2.2.1 General properties of effector functions of antibodies <br />Locations of antibody functioning<br />Production of antibody<br />Activation of antibody function<br />Antibody functions<br />5.2.2.2 Types of effector functions of antibodies<br />Antibody neutralization of microbe and toxins<br />Antibody-mediated opsonization and phagocytosis<br />Antibody-dependent cellular cytotoxicity<br />Complement activation(classical pathway)<br />5.2.2.3 Effector functions of antibodies at special anatomic sites<br />mucosal immunity<br />neonatal immunity<br />5.3 Connections between innate and adaptive immunitgy<br />6. Regulation of Immune reponses<br />6.1 Cytokines and their receptors<br />6.1.1 Cytokines<br />6.1.1.1 General properties of cytokines<br />6.1.1.2 Classifications of cytokines<br />According to cell resources<br />According to the functions<br />Based on their principle biologic actions:<br />Based on their immunological roles:<br />6.1.1.3 Functional categories of cytokines<br />Cytokines that mediate and regulate innate immunity<br />TNF<br />Chemokines<br />Type I IFN (a and b)<br />Interleukin<br />IL-1<br />IL-12<br />IL-10<br />others<br />Cytokines that mediate and regulate adaptive immunity<br />Interleukin<br />IL-2<br />IL-4<br />IL-5<br />Type II IFN (g)<br />Growth factor<br />others<br />Cytokines that stimulate hematopoiesis<br />Stem cell factor<br />Interleukin<br />IL-7<br />IL-3<br />6.1.2 Cytokine receptors<br />6.1.2.1 Classifications of cytokine receptors<br />Ig super family<br />Class I cytokine receptors<br />Class II cytokine receptors<br />TNF receptors<br />Chemokine receptors<br />6.1.2.2 Examples of most studied cytokine receptors<br />IL-2R<br />IL-15R<br />mode of reaction<br />The same cell both produces and transpresents IL-15<br />Transregulation of memory CD8 T-cell proliferation by IL-15Ralpha+ bone marrow-derived cells<br />receptor shedding<br />6.1.3 Cytokine signaling pathways<br />6.1.3.1 JAK-STAT pathways<br />6.1.3.2 IFN signaling pathway<br />6.1.4 Regulation of cytokine production and functions<br />6.1.4.1 Cytokine Antagonists<br />6.1.4.2 Cytokine Secretion by TH1and TH2 CD4 T cells Subsets<br />The Development of TH1 and TH2 Subsets Is Determined by the Cytokine Environment<br />Cytokine Profiles Are Cross-Regulated<br />6.1.4.3 Cytokine diseases <br />Diseases caused by Th1/Th2 cytokine imbalance<br />Bacterial Septic or Toxic shock<br />6.1.4.4 cytokine-based therapy<br />6.2 Immunological Memory<br />6.2.1 T cell memory<br />6.2.1.1 CD8 T cell clssification<br />6.2.1.2 T cells memory development<br />Antigen persistence<br />Signals strength<br />Regulation of genes<br />Time course<br />Other tid-bits<br />6.2.1.3 T cells memory functions: linking “memory” to “protection<br />6.2.1.4 T cell memory maintenance and longevity<br />6.2.1.5 Effect of heterologous infections on memory<br />6.2.2 B cell memory<br />6.2.2.1 B cells memory and plasma cells development<br />anitgen persistence<br />plasma cell ontogeny<br />6.2.2.2 B memory cell activation<br />6.2.2.3 B cell memory maintenance and longevity<br />6.3 Immunologic tolerance (inactivation of lymphocytes) <br />6.3.1 General feature and mechanismof immunologic tolerance <br />6.3.2 Self Tolerance<br />6.3.2.1 Central tolerance<br />Central T cell tolerance<br />Positive selection<br />Negative selection<br />Central B cell tolerance<br />6.3.2.2 Peripheral tolerance<br />Peripheral T cell tolerance<br />Anergy <br />induced by lack of costimulation<br />induced by inhibitory receptors<br />Deletion <br />activation-induced cell death(fas-mediated)<br />quot;
passive cell death (fail to encounter self-antigen)<br />Terminal signaling<br />Inhibited by Regulatory T cells<br />Perpheral B cell tolerance<br />6.3.3 Foreign Tolerence<br />6.3.3.1 Factors that determine the tolerogenicity of protein antigens<br />6.3.3.2 Induction and Breaking Tolerance<br />Induction of Tolerance<br />Oral tolerance<br />Soluble-peptide tolerance<br />Fixed-cell tolerance<br />Co-stimulatory blockade<br />Breaking Tolerance<br />6.3.4 Homeostasis: termination of normal immune responses<br />6.3.5 Autoimmune Diseases<br />6.3.5.1 Multiple sclerosis(MS)<br />6.3.5.2 R-EAE<br />6.3.5.3 TMEV-IDD<br />6.4 New subsets of CD4 T cells: Regulotary T cells(Tregs) and Th17 effector CD4 T cells<br />6.4.1 Treg<br />6.4.1.1 General properties<br />6.4.1.2 Different regulatory T cells<br />Foxp3+ Natural Treg(contact)<br />Foxp3+ adaptive Treg(TGFb)<br />Foxp3- adaptive Treg(IL10)<br />6.4.2 Th17<br />6.4.2.1 Identification of Th17<br />6.4.2.2 Th17 in EAE<br />6.4.2.3 Antagonism of Th17<br />7. Inflammation and Leukocytes migration<br />7.1 Inflammation<br />7.1.1 Initiation of inflammation<br />7.1.2 Acute inflammation<br />7.1.2.1 Main features of acute inflammation<br />vasodilation<br />increased vascular permeability<br />leukocytes recruitment and activation<br />fever<br />7.1.2.2 Local and systemic acute inflammation<br />local inflammation<br />systemic inflammation<br />7.1.2.3 Mediators of acute inflammation<br />Molecular mediators<br />The Plasma Proteases<br />Lipid Mediators<br />Peptides and Amines<br />Nitric Oxide<br />Acute-Phase Reactants<br />Proinflammatory Cytokines<br />Novel Mediators: Leptin and Lipocalins<br />Cell mediators<br />Neutrophils<br />Monocytes and Macrophages<br />Eosinophils<br />Platelets and Lymphocytes<br />Endothelial and Epithelial Cells<br />7.1.3 Chronic inflammation<br />7.1.3.1 Features of acute inflammation<br />7.1.3.2 Chronic inflammation diseases<br />7.1.4 Anti-Inflammatory Agents<br />7.1.4.1 Antibody Therapies<br />7.1.4.2 Corticosteroids<br />7.1.4.3 NSAIDs<br />7.2 Cell-Adhesion Molecules(CAM)<br />7.2.1 Families of CAM<br />7.2.1.1 SELECTINS<br />7.2.1.2 MUCINS<br />7.2.1.3 INTEGRINS<br />7.2.1.4 ICAMS<br />7.2.2 Functions of CAM<br />7.3 Chemokines—Key Mediators of Inflammation<br />7.3.1 Families of chemokines and chemokine receptors<br />7.3.2 functions and mechanims of chemokines<br />7.4 Leukocytes migration<br />7.4.1 Neutrophil Extravasation<br />7.4.1.1 Step 1: Tethering & rolling<br />7.4.1.2 Steps 2 & 3: Activation & arrest<br />activation<br />arrest<br />7.4.1.3 Step 4:Migration and diapedesis<br />Diapedisis: pathways of lymphocyte migration across endothelial cells<br />migration<br />7.4.2 Lymphocytes Extravasation and Recirculation<br />7.4.2.1 Lymphocyte extravsation<br />High-Endothelial Venules and post-capillary venules<br />Adhesion-Molecule Interactions<br />How do lymphocyte move<br />7.4.2.2 Lymphocyte circulation<br />Naive lymphocytes recirculate to secondary lymph node tissue<br />Inflammation-induced lymphocyte recirculation<br />induction of inflammation <br />Innate Signals Are Sufficient to Induce Lymph Node Hypertrophy<br />Inflammation Induces Recruitment of Nondividing Naive Lymphocytes to the dLN<br />Inflammation-Induced Recirculation Occurs via the High Endothelial Venule(HEV)<br />Effector and Memory Lymphocytes Adopt Different Trafficking Patterns(Tissue specificity and imprinting of lymphocyte migration)<br />Tissue-specific DCs<br />Specific homing phenotype of lymphocytes<br />Tissue specific microenvironments determines the homing phenotype of lymphocytes<br />Adoptive cell transfer experiment<br />Stromal cell networks<br />7.4.2.3 Regulatory molecules in lymphocyte circulation<br />Tetinoic acid<br />S1P1(S1P receptor) is necessary for lymphocyte egress from LN<br />mechanism of sequestrating drug FTY270(S1P agonist)<br />S1P1-/- T and B cells fail to accumulate in secondary lymphoid tissue<br />CD69 acts downstream of interferon-a/b to inhibit S1P1 and lymphocyte egress from lymphoid organs<br />8. Mucosal immunology<br />8.1 General properties of the mucosal immune system<br />8.2 Components and structure of mucosal immune system<br />8.2.1 Small intestinal structure<br />8.2.2 Gut associated lymphoid tissues(GALT)<br />8.2.2.1 M cells<br />8.2.2.2 Intraepithelial Lymphocytes (IEL)<br />8.2.2.3 Intestinal epithelial cells (IECs)<br />8.2.2.4 DC<br />8.2.2.5 Lamina propria lymphocytes<br />T cells<br />B cells and IgA<br />8.3 Antigenic challenge and immune responses in intesitine<br />8.3.1 Antigenic challenge in intestine<br />8.3.2 Immune responses in intesitine<br />8.3.2.1 Commensals vs pathogens<br />Commensals protect epithelial damage via TLR pathway<br />Limited penetration of commensals insured by mucosal immune system<br />Commensal loaded DCs can induce IgA<br />Penetration of E. cloacae after intestinal challenge.<br />8.3.2.2 Food tolerance<br />9. Immune Defences<br />9.1 Immunity to Infectious Agents<br />9.1.1 Immunity to Bacteria<br />9.1.1.1 General Aspects of Bacterial<br />Bacterial adherence and Colonization<br />Potential Colonization Sites<br />Ways of adherence<br />Bacterial virulence factors<br />Bacterial infection<br />Rout of infection<br />Spread of Infection<br />Extracellular vs intracellular bacteria<br />Host primary physical and chemical barrier defense<br />9.1.1.2 Extracellular bacteria<br />Immunity against extracellular bacteria<br />innate immune response<br />adaptive response<br />Invade mechanisms by extracellular bacteria<br />Avoiding phagocytosis<br />Toxins<br />Delivery of toxins<br />Effect of toxin<br />Toxic shock syndrome<br />Toxicity of LPS<br />Example of extracellular bacteria:Helicobacter pylori<br />H. pylori Virulence Factors<br />VacA<br />CagA<br />Hp LPS – Immune Mimicry<br />Peptidoglycan (PGN)<br />immune response to H.pylori<br />9.1.1.3 Intracellular bacteria<br />Immunity against intracellular bacteria<br />humoral response<br />cell mediated response<br />innate cell-mediated response<br />adaptive cell-mediated response<br />Invasion mechanism of intracellular bacteria<br />Phagocytosis<br />clatherin-independent<br />“Zippering” method of internalization<br />Ruffling method of internalization<br />M cell Internalization<br />Survival Strategies within Phagocytes<br />Example of intracellular bacteria: salmonella<br />9.1.1.4 Diseases and pathogenesis by bacteria<br />Damage from immune response<br />Diphtheria (Corynebacterium diphtheriae)<br />Tuberculosis (Mycobacterium tuberculosis)<br />9.1.2 Immunity to Virus<br />9.1.2.1 Host immune response to virus<br />innate immune response<br />adaptive immune response<br />9.1.2.2 Mechanisms of immune evasion by virus<br />Escape by Mutations<br />Escape by Hiding<br />Escape by Latency<br />Escape by Destruction of Immune Cells<br />Escape by Subverting Antigen Processing and Antigen Presentation<br />Inhibition of T Cell-Mediated Target Cell Lysis<br />Inhibition of Natural Killer Cell Activity<br />Inhibition of Complement Activation<br />Interference of Cytokine Functions<br />Crystallized Fragment (Fc) Receptor Mimetics<br />9.1.3 Immunity to Parasites<br />9.1.3.1 Nature of parasitic pathogens<br />9.1.3.2 Host Immune responses to parasites<br />innate immune response<br />adaptive immune response<br />9.1.3.3 Mechanism of immune evasion by parasites<br />9.1.3.4 Anti-malarial immunity and pregnancy<br />Malaria biology<br />Introduction<br />Life cycle<br />Malaria during pregnancy<br />Pathogenesis of malaria<br />Placental Cytoadherence<br />Antigen Variation<br />Immunogenesis of malaria<br />T cell responses<br />Humoral responses<br />9.2 Immunity to Transplantation <br />9.2.1 Immunologic Basis of Graft Rejection<br />9.2.1.1 Types of transplants and graft rejection<br />9.2.1.2 Properties of graft rejection<br />Allograft Rejection Displays Specificity and Memory<br />Similar Antigenic Profiles Foster Allograft Acceptance<br />Cell-Mediated Graft Rejection Occurs in Two Stages<br />Graft Donors and Recipients Are Typed for RBC and MHC Antigens<br />9.2.2 Immune response to allogenenic transplantation<br />9.2.2.1 Alloantigens presentation by recognition of T cells<br />direct presentation of alloantigens<br />indirect presentation of alloantigens<br />9.2.2.2 Activation of alloreactive T cells <br />CD4 /CD8 T cell activation in vivo<br />mixed lymphocyte reaction(MLR)<br />9.2.2.3 Effector mechanisms of allograft rejection<br />9.2.3 Clinical Manifestations of Graft Rejection <br />9.2.3.1 Hyperacute rejection<br />9.2.3.2 Acute rejection<br />9.2.3.3 Chronic rejection<br />9.3 Immunity to tumors<br />9.3.1 Cancer: Origin and Terminology<br />9.3.1.1 Origin of Cancer<br />9.3.1.2 Cancer associated genes<br />9.3.1.3 Cancer induction process<br />9.3.2 Tumor immunology<br />9.3.2.1 Tumor antigens<br />Identification of tumor antigens<br />Two types of tumor antigens<br />Tumor-specific transplantation antigens(TSTAs)<br />products of mutated oncogenes and tumor suppressor genes<br />products of other mutated genes<br />tumor antigens encoded by genomes of oncogenic viruses<br />Tumor-associated transplantation antigens(TATAs)<br />overexpressed and abnormally expressed cellular proteins<br />altered glycolipid and glycoprotein antigens<br />Tissue-specific differentiation antigens<br />oncofetal antigens<br />9.3.2.2 Immune response to tumors<br />NK cells<br />macrophages<br />T cells<br />antibodies<br />9.3.3 Tumor Evasion of immune response<br />10. Immune Diseases <br />10.1 Hypersensitivity and Autoimmune diseases(Abnormal immune responses) <br />10.1.1 Effector mechanisms of abnormal immune responses and diseases<br />10.1.1.1 Antibody mediated<br />Antibody-mediated<br />Antibody-antigen complex mediated<br />10.1.1.2 T cells mediated<br />10.1.2 Hypersensitivity diseases<br />10.1.2.1 Causes of hypersensitivity<br />10.1.2.2 Types of hypersensitivity<br />Type I: IgE antibody mediated Immediate Hypersensitivity (uncontrolled or excessive responses against foreign antigens)<br />Components of type I hypersensitivity<br />Allergens<br />REAGINIC ANTIBODY (IgE)<br />Mast cells, basophils and eosinophile<br />IgE-BINDING Fc RECEPTORS<br />Sequence of events<br />Production of IgE<br />Binding of IgE to IgE Fc receptor on Mast cells and Basophiles<br />Activation of effector cells<br />Activation of Mast cells<br />Mediators produced by effector cells<br />Regulation of mast cell degranuation<br />Biological effect<br />Two effector phases of type I hypersensivity reactions<br />Early phase reaction(immediate)<br />Late phase reactions(2-4hours)<br />Detect Type I Hypersensitivity Reactions<br />Type I hypersensitivity diseases and therapies<br />Systemic/loclized anaphylaxis<br />SYSTEMIC ANAPHYLAXIS<br />LOCALIZED ANAPHYLAXIS (ATOPY)<br />ALLERGIC RHINITIS<br />Bronchial Asthma<br />Allergies of skin, upper respiratory and gut<br />Therapies<br />immunotherapy<br />therapeutic drugs<br />Pathogenesis of type I hypersensitivity<br />Genetic susceptibility<br />Hygene hypothesis<br />Type II: IgG antibody mediated Cytotoxic Hypersensitivity (immune antibody response against self-antigen) <br />Blood Transfusion Reactions<br />Hemolytic Disease of the Newborn<br />Drug-Induced Hemolytic Anemia<br />Type III: Antibody-antigen complex mediated Hypersensitivity (self antigens or foreign antigens with bound antibody)<br />Type IV: T cell mediated Hypersensitivity(Delayed type hypersensitivity, DTH): autoimmune response or response to foreign antigens <br />Effector functions<br />Phases of reaction<br />Detection<br />Diseases<br />10.1.3 Autoimmune diseases<br />10.1.3.1 General properties of autoimmune disease<br />10.1.3.2 Types of autoimmune diseases<br />Organ specific autoimmune diseases<br />Mediated by Direct Cellular Damage<br />Mediated by Stimulating or Blocking Auto-Antibodies<br />Systemic autoimmune diseases<br />10.1.3.3 Proposed mechanism for induction of autommune diseases<br />Genetic basis of autoimmune disease<br />Role of infections in autoimunity<br />Release of Sequestered Antigens Can Induce Autoimmune Disease<br />Inappropriate Expression of Class II MHC Molecules Can Sensitize Autoreactive T Cells<br />Polyclonal B-Cell Activation Can Lead to Autoimmune Disease<br />10.2 Congenital and acquired immunodeficiencies (Lack of immune responses)<br />10.2.1 Congenital(Primary) immunodeficiencies<br />10.2.1.1 Defects in innate immunity<br />defect in microbicidal activities of phagocytes<br />leukocyte adhesion deficiencies<br />defect in NK cells and other leukocytes: the Chediak-Higashi syndrom<br />10.2.1.2 Defects in adaptive immunity<br />Defects in lymphocytes maturation<br />disorder of both B and T cells(severe combined immunodeficiencies, SCIDs)<br />X-linked SCID caused by mutation of the cytokine receptor commom g chain<br />SCID caused by Adenosine deaminase deficiency<br />defect in B cell maturation: X-linked agammaglobulinemia<br />defect in T cell maturation: DiGeorge syndrome<br />Defects in lymphocytes activation and function<br />defect in B cell activation and function<br />selective immunoglobulin isotype deficiencies<br />defects in B cell differentiation: common variable immunodeficiency<br />defect in T cell activation and function<br />Defect in T cell-dependent B cell activation: the X-linked hype-IgM syndrom<br />defects in T cell activation and function<br />Defects in MHC expression<br />10.2.2 Acquired(Secondary) immunodeficiencies<br />10.2.2.1 Pathogenic mechanisms<br />10.2.2.2 HIV and the Acquired Immunodeficiency Syndrome(AIDS)<br />Molecular and biologic features of HIV<br />HIV structure and Genes<br />Viral life cycle<br />entry<br />replication and regulation<br />package<br />The course of HIV disease<br />HIV infection<br />Steps in HIV infection and pathogenesis<br />HIV reservoirs and viral turnover<br />immune responses to HIV<br />mechanism of immunodeficiency<br />immune evasion by HIV<br />Treatment and prevention of AIDS<br />11. Immunotherapy: Manipulation of immune responses<br />11.1 Activation of immune respones<br />11.1.1 Vaccination against infectious agents<br />11.1.1.1 Introduction<br />History of vaccine<br />Terminology of vaccination<br />Vaccine Classifications<br />Vaccines of two different strategies <br />Three basic vaccines<br />Other vaccines<br />11.1.1.2 Passive and active immunization<br />Passive immunization<br />Common agents of passive immunization<br />Conditions that warrant the use of passive immunization<br />Advantage and disadvantage<br />Active immunization<br />Natrual infection<br />Vaccination programs<br />Vaccines for use in humans to date<br />Vaccines used in National Immunization Programs<br />11.1.1.3 Requirements for effective vaccination<br />Vaccine types<br />Whole organism vaccine<br />Live attenuated vaccine<br />Inactivated vaccine<br />Subunit vaccine<br />DNA vaccine<br />Recombinant viral vector DNA vaccine<br />Recombinant plasmid DNA vaccine<br />Peptide vaccine<br />immunogenic peptide identification<br />problems and overcomes<br />TI antigen and conjugate vaccine<br />Adjuvant<br />microbial constituents<br />Complete Freund's Adjuvant(CFA)<br />Bacterial toxins(CT,LT) and derivatives<br />CpG containing DNA<br />Cytokines/chemokines<br />Live vectors<br />virus like particles<br />adjuvant as particulate delivery systems<br />micorspheres<br />liposomes<br />lipopeptides<br />single chain lipid<br />clustered lipid chain<br />Lipid core peptide(LCP) system<br />Rout of vaccination<br />11.1.1.4 Designing of therapeutic vaccine to control existing chronic infections<br />Two cases of chronic infections<br />Treatment of chronic infections<br />11.1.2 Tumor immunotherapy<br />11.1.2.1 Active immunotherapy<br />vaccination with tumor cells and tumor antigens<br />augmentation of host immunity to tumors by using cytokines and costimulators transfected tumor cells<br />nonspecific stimualtion of the immune system<br />11.1.2.2 Passive immunotherapy<br />Therapy with anti-tumor antibodies<br />Adoptive cellular therapy<br />11.2 Suppression of immune responses<br />11.2.1 Immune tolerance or supression of allograft transplatation<br />11.2.1.1 Immunosupression therapy of allograft rejection<br />General immunosuppressive therapy<br />Immunosuppression of T cells<br />plasmaphoresis<br />anti-inflammatory agents<br />Mitotic Inhibitors<br />Total Lymphoid Irradiation EliminatesLymphocytes<br />Specific immunosuppressive therapy<br />Monoclonal Antibodies Can Suppress Graft-Rejection Responses<br />Blocking Co-Stimulatory Signals to Induce Anergy<br />11.2.1.2 Immune tolerance to allograft<br />11.2.2 Immunotherapy of hypersensitivity<br />11.2.3 Immunotherapy of autoimmune diseases<br />11.2.3.1 T-Cell Vaccination Is a Possible Therapy<br />11.2.3.2 Some experimental agents for immunointervention<br />11.2.3.3 Oral Antigens Can Induce Tolerance<br />Immunolgy 1.1.1 Overview of immune responses in vivo 1.1.2 Classification 1.1.2.1 innate and adaptive immunity Innate immune response stimulates adaptive immune responses. Adaptive immune enhances innate immunity.They are components of an integrated system of host defense system.Innate immunity also called natural or native immunity: cellular and biochemical defense mechanisms that are in place before infection and respond rapidly to infections.Components:physical and cheical barriers:skin, mucosal epithelia,antimicrobial chemicalsblood proteins: complementcells: phagocytesadaptive immunity stimulated by exposure to infectious agents and increase in magnitude and defensive capabilities with each successive exposure to a particular antigens.features Specificity and Memory :mount heightened response to persist infection of the same antigen.A substantial specific response takes TIME & ENERGY.Diversity: Respond in distinct and special ways to different micobes which enables the host to quot;
custom designquot;
responses to best combat many different types of microbes.specialization: Respond in distinct and special ways to different micobes which enables the host to quot;
custom designquot;
responses to best combat many different types of microbes.self-limitation: Return to resting basal state, called homeostatsis, after antigen stimulationself-nonreactivity: also called self-tolerance. prevent to react against one's own cells.phases 5 phases:recognition of antigenactivation of lymphocytesantigen elimination (effector phase)homeostasismemory1.1.2.2 humoral and cell-mediated immunity humoral immunity mediated by molecules in the blood and mucosal secretions.called antibodies,that are produced by B cells.principal defense against extracellular microbescell-mediated immunity mediated by T lymphocytes.principal defense against intracellular microbes.1.1.2.3 active and passive immunity active immunity: protective immunity induced by exposure to a foreign antigen.passive immunity:protective immunity gained by tranfering antibodies or lymphocytes specific for an antigen without ever having been exposed to or having respond to that antigens. <br /> <br />