Immunological synapse
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The immunological synapse is the contact point between a T cell and antigen presenting cell where signaling and protein segregation occurs. It is composed of concentric rings called the central, peripheral, and distal supramolecular activation complexes. Signaling occurs through redistribution and segregation of receptors and proteins at the cell surface through both passive binding and active lateral movement and vesicle transport. Immunological synapses play a role in processes like HIV persistence through virological synapse formation between infected and uninfected T cells.
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Immunological synapse
The immunological synapse is a specialized signaling structure formed at the interface between T lymphocytes and antigen presenting cells. It consists of three main components: T cell receptors, adhesion molecules, and co-stimulatory molecules. Formation of the mature immunological synapse involves molecular redistribution through diffusion and cytoskeletal movement over 5-30 minutes, resulting in a structure with central, peripheral, and distal supramolecular activation clusters that facilitate T cell signaling and activation. This signaling activates transcription factors that induce cytokine gene expression and T cell effector functions.
Tcr
Altering the specificity of T cell receptor (TCR) is one of the popular strategies to genetically modify T cells to enhance the tumor-killing activity of T cells. From a tumor-reactive T cell or active anti-tumor T-cell antigens, the appropriate target sequence is introduced to modify T cells to target a broad range of tumors with improved specificity. https://www.creative-biolabs.com/car-t/cellrapeutics-tcr-technology.htm
T CELL ACTIVATION AND IT'S TERMINATION
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.
Cell-mediated immune responses
This document summarizes cell-mediated immune responses by T lymphocytes. It discusses:
1) The phases of T cell responses including antigen recognition, costimulation, differentiation into effector cells, and signal attenuation.
2) How T cells recognize antigens through the T cell receptor complex and costimulatory molecules help activate T cells.
3) The roles and mechanisms of effector T cell subsets like Th1, Th2, and cytotoxic CD8+ T cells in fighting infection through secretion of cytokines and direct killing of infected cells.
4) How effector T cells migrate and are retained at sites of infection through adhesion molecules and homing receptors.
Cells & organs ofthe immune system
The document summarizes key aspects of the immune system. It describes how the immune system is made up of cells that develop in primary lymphoid organs like the bone marrow and thymus. Mature cells then travel to secondary lymphoid organs like lymph nodes and spleen. These organs contain various white blood cells that participate in immune responses, developing from hematopoietic stem cells in bone marrow through processes like apoptosis and regulation by genes and cytokines.
T CELL RECEPTOR.pptx
The T cell receptor (TCR) is a protein complex found on the surface of T cells that is responsible for recognizing fragments of antigen bound to MHC molecules. It consists of an alpha and beta chain, with 95% of T cells containing these chains and 5% containing gamma and delta chains instead. Each chain contains a variable region that binds the peptide-MHC complex and a constant region near the cell membrane. The variable regions contain three hypervariable complementarity-determining regions important for antigen recognition. The TCR is associated with CD3 proteins that transmit activation signals into the T cell upon peptide binding. TCR diversity arises from genetic recombination of DNA segments during T cell development.
B CELL RECEPTOR final.pptx
The B cell receptor is a transmembrane protein on B cells that is composed of a membrane-bound immunoglobulin molecule and a signal transduction moiety. The B cell receptor consists of an Ig molecule anchored to the cell's surface and has two key functions: signal transduction upon antigen interaction and internalization of antigens for processing and presentation to T cells. The B cell co-receptor is a complex of CD19, CD21, and CD81 expressed on mature B cells.
Antigen Recognition
T lymphocytes recognize short peptide fragments of proteins bound to major histocompatibility complex (MHC) molecules on the surface of antigen-presenting cells. There are two classes of MHC molecules - MHC class I presents peptides to CD8+ T cells on all nucleated cells, while MHC class II presents peptides to CD4+ T cells on professional antigen-presenting cells. Peptides bind to MHC molecules through anchor residues in a specific sequence motif, and a single MHC molecule can bind many different peptides. MHC molecules are highly polymorphic, which limits T cell recognition to peptides bound to self MHC molecules only.
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Immunological synapse
The immunological synapse is a specialized signaling structure formed at the interface between T lymphocytes and antigen presenting cells. It consists of three main components: T cell receptors, adhesion molecules, and co-stimulatory molecules. Formation of the mature immunological synapse involves molecular redistribution through diffusion and cytoskeletal movement over 5-30 minutes, resulting in a structure with central, peripheral, and distal supramolecular activation clusters that facilitate T cell signaling and activation. This signaling activates transcription factors that induce cytokine gene expression and T cell effector functions.
Tcr
Altering the specificity of T cell receptor (TCR) is one of the popular strategies to genetically modify T cells to enhance the tumor-killing activity of T cells. From a tumor-reactive T cell or active anti-tumor T-cell antigens, the appropriate target sequence is introduced to modify T cells to target a broad range of tumors with improved specificity. https://www.creative-biolabs.com/car-t/cellrapeutics-tcr-technology.htm
T CELL ACTIVATION AND IT'S TERMINATION
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.
Cell-mediated immune responses
This document summarizes cell-mediated immune responses by T lymphocytes. It discusses:
1) The phases of T cell responses including antigen recognition, costimulation, differentiation into effector cells, and signal attenuation.
2) How T cells recognize antigens through the T cell receptor complex and costimulatory molecules help activate T cells.
3) The roles and mechanisms of effector T cell subsets like Th1, Th2, and cytotoxic CD8+ T cells in fighting infection through secretion of cytokines and direct killing of infected cells.
4) How effector T cells migrate and are retained at sites of infection through adhesion molecules and homing receptors.
Cells & organs ofthe immune system
The document summarizes key aspects of the immune system. It describes how the immune system is made up of cells that develop in primary lymphoid organs like the bone marrow and thymus. Mature cells then travel to secondary lymphoid organs like lymph nodes and spleen. These organs contain various white blood cells that participate in immune responses, developing from hematopoietic stem cells in bone marrow through processes like apoptosis and regulation by genes and cytokines.
T CELL RECEPTOR.pptx
The T cell receptor (TCR) is a protein complex found on the surface of T cells that is responsible for recognizing fragments of antigen bound to MHC molecules. It consists of an alpha and beta chain, with 95% of T cells containing these chains and 5% containing gamma and delta chains instead. Each chain contains a variable region that binds the peptide-MHC complex and a constant region near the cell membrane. The variable regions contain three hypervariable complementarity-determining regions important for antigen recognition. The TCR is associated with CD3 proteins that transmit activation signals into the T cell upon peptide binding. TCR diversity arises from genetic recombination of DNA segments during T cell development.
B CELL RECEPTOR final.pptx
The B cell receptor is a transmembrane protein on B cells that is composed of a membrane-bound immunoglobulin molecule and a signal transduction moiety. The B cell receptor consists of an Ig molecule anchored to the cell's surface and has two key functions: signal transduction upon antigen interaction and internalization of antigens for processing and presentation to T cells. The B cell co-receptor is a complex of CD19, CD21, and CD81 expressed on mature B cells.
Antigen Recognition
T lymphocytes recognize short peptide fragments of proteins bound to major histocompatibility complex (MHC) molecules on the surface of antigen-presenting cells. There are two classes of MHC molecules - MHC class I presents peptides to CD8+ T cells on all nucleated cells, while MHC class II presents peptides to CD4+ T cells on professional antigen-presenting cells. Peptides bind to MHC molecules through anchor residues in a specific sequence motif, and a single MHC molecule can bind many different peptides. MHC molecules are highly polymorphic, which limits T cell recognition to peptides bound to self MHC molecules only.
Major Histocompatibility complex & Antigen Presentation and Processing
The document discusses the major histocompatibility complex (MHC) and antigen processing and presentation. It describes MHC molecules as polymorphic glycoproteins that play a role in discriminating self from non-self and participate in both humoral and cell-mediated immunity. MHC class I molecules present endogenous antigens on most nucleated cells and interact with CD8+ T cells. MHC class II molecules present exogenous antigens on antigen-presenting cells and interact with CD4+ T cells. Antigens are processed into peptides of appropriate size and bound motifs to be presented in the binding groove of MHC molecules.
B Cell Development
- B cell development begins with stem cells in the bone marrow, where they undergo a series of differentiation stages defined by immunoglobulin gene rearrangement under the influence of cytokines and contact with stromal cells.
- Successful rearrangement of the heavy and light chain genes leads to expression of a B cell receptor (BCR) and selection of clones that do not recognize self-antigens through deletion, anergy or receptor editing.
- Mature B cells that pass self-tolerance checkpoints are exported from the bone marrow to the peripheral immune system.
The T-Cell Antigen Receptor Complex
The document summarizes key points about the T-cell antigen receptor complex:
1) The T-cell receptor (TCR) is highly variable between individuals due to small changes in charge and shape at its ends, which allows it to recognize a diverse range of peptide antigens bound to MHC molecules.
2) TCR diversity is generated through combinatorial and junctional mechanisms similar to immunoglobulin genes, including the use of multiple variable, diversity and joining gene segments.
3) Unlike antibodies, TCRs do not undergo somatic mutation, which helps prevent autoimmunity by ensuring TCRs maintain recognition of peptide-MHC complexes.
T-Cell Mediated Immunity
T cells are activated through the recognition of antigen peptides presented on MHC complexes on antigen presenting cells (APCs). This leads to T cell proliferation and differentiation into effector T cells. Cytotoxic T cells recognize endogenous antigens on MHC I to kill infected cells, while helper T cells recognize exogenous peptides on MHC II and secrete cytokines to stimulate macrophage activation or B cell antibody production. Full T cell activation requires both antigen recognition by the TCR and co-stimulatory signaling between molecules such as B7 and CD28.
Antigens and immunogens immunogenecity
Immunogens are substances that can induce an immune response, while antigens are substances that can bind to antibodies or T-cell receptors. Not all antigens are immunogenic. The properties of an effective immunogen include foreignness, molecular size over 100,000 Daltons, chemical complexity, and the ability to be processed and presented by antigen-presenting cells. The immunogenicity of a substance depends on additional factors like dosage, route of administration, use of adjuvants, and host genetics. Antigens can be classified as exogenous, endogenous, autoantigens, or complete versus incomplete antigens.
T-cell activation
T-Cell Activation
• Concept of immune response
• T cell-mediated immune response
• B cell-mediated immune response
I. Concept of immune response
• A collective and coordinated response to the introduction of foreign substances in an individual mediated by the cells and molecules in the immune system.
II. T cell-mediated immune response
• Cell-mediated immunity is the arm of the adaptive immune response whose role is to combat infection of intracellular pathogens, such as intracellular bacteria (mycobacteria, listeria monocytogens), viruses, protozoa, etc.
Immunotolerance: mechanism and consequence
The document discusses several key mechanisms by which the immune system maintains tolerance to self-antigens to avoid autoimmunity. These include central tolerance in the thymus through negative selection which deletes self-reactive T cells, peripheral tolerance through ignorance, anergy, suppression and regulatory T cells, and the concept that tolerance is the default response unless danger signals are present to trigger an immune response. The timing of antigen exposure is also important, as antigens encountered during early development are more likely to induce tolerance.
Tumor immunology
This document discusses tumor immunology and cancer immunotherapy. It provides information on tumor antigens, how tumors stimulate an immune response, and mechanisms tumors use to evade the immune system. The document also outlines several approaches to cancer immunotherapy, including monoclonal antibodies, cytokines, and adoptive cell therapy. A brief history of cancer immunotherapy is given, noting early experiments in the 1890s using bacterial toxins to treat tumors and discoveries in the 1960s about antibody receptors and T cells recognizing cancer cells.
Tregs
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.
Mhc
The document discusses major histocompatibility complexes (MHCs), which are glycoproteins found on cell surfaces that present antigen fragments to T cells. It describes MHC Class I and Class II molecules, which present antigens from intracellular and extracellular pathogens, respectively. MHC genes were first identified as important in tissue graft rejection and show high polymorphism between individuals.
Tcr class
T-cell receptors are heterodimers consisting of alpha and beta chains with variable and constant regions. The variable region binds to antigens presented by the major histocompatibility complex and contains complementary determining regions that provide specificity. While the TCR is responsible for antigen recognition, it does not signal within the cell itself. Signal transduction is carried out by the CD3 complex, which contains gamma, delta, epsilon, and zeta chains and lacks kinase activity.
B cell Activation by T Independent & T Dependent Antigens-Dr C R Meera
During humoral immune response, Ab production is brought about by B lymphocytes. Based on the ability to induce Ab formation, antigens can be classified into T independent and T dependent antigens. Some antigens can directly induce the B cells to produce the Abs and are called T Independent Ans. However, some Ans require the help of T lymohocytes for the production of Abs from B cells. These Ans are called T Dependent Ans.
MHC and TCR
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.
Somatic hypermutation
Somatic hypermutation (SHM) introduces mutations in antibody genes in B cells, increasing antibody diversity and affinity for antigens. SHM occurs through the actions of activation-induced cytidine deaminase and other molecules at a rate of 10-3 mutations per base pair, compared to the typical spontaneous mutation rate of 10-8 per base pair. These mutations mainly occur in hypervariable regions of antibody genes and result from nucleotide substitutions. SHM leads to affinity maturation of B cells and increased antibody affinity for antigens. Future directions include using the SHM process to evolve proteins in mammalian cells.
Major Histocompatibility Complex
Some potential causes of the immune system attacking the self in autoimmune diseases include:
- Genetic predisposition - Genes coding for the variety of MHC molecules can influence susceptibility. A T cell's ability to respond is determined by MHC genotype. Differences in MHC alleles' ability to present autoantigens can play a role.
- Environmental triggers - Factors like infections, drugs, trauma, etc. may trigger autoimmunity in genetically susceptible individuals by molecular mimicry or other mechanisms.
- Loss of tolerance - Failure to eliminate self-reactive lymphocytes during development or maintain peripheral tolerance can allow self-reactivity.
- Hormonal factors - Many autoimmune diseases are more common in women and fluctuate with horm
MHC MOLECULES
The document discusses the major histocompatibility complex (MHC) in mammals. It notes that MHC acts as antigen presenting receptors and are involved in cell-cell interaction, antigen presentation, and recognition of self and non-self molecules. MHC is found on chromosome 6 in humans and is referred to as the HLA complex. MHC molecules are divided into three main classes - Class I MHC present antigens to cytotoxic T cells, Class II MHC present antigens to helper T cells, and Class III MHC genes encode complement components and cytokines. The structures and functions of Class I and Class II MHC molecules are described in detail.
Chapter 5 Immunology
T cells recognize antigens presented by MHC molecules on other cells. Antigens from intracellular sources such as viruses are processed and presented by MHC class I to CD8+ T cells. Antigens from extracellular sources such as bacteria that are endocytosed are processed and presented by MHC class II to CD4+ T cells. The antigen processing pathways and the classes of MHC molecules that present the peptides allow the immune system to mount appropriate responses targeting different types of pathogens.
Major histocompatibility complex
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.
Complement system
The document discusses the complement system of teleost fish. It has three pathways - the classical pathway, lectin pathway, and alternative pathway. All three pathways involve a cascade of complement components that ultimately lead to the formation of the membrane attack complex (MAC) on pathogen surfaces. The MAC forms pores that lyse pathogens. The complement system also opsonizes pathogens and generates inflammatory peptides like C3a and C5a. Strict regulation is needed to prevent damage to host cells, mediated by factors such as C1 inhibitor, factor H, decay accelerating factor, and CD59.
T cell signalling pathway
The T cell receptor signaling pathway involves T cells binding antigens presented by MHC proteins on antigen presenting cells. When the T cell receptor binds to its antigen, it activates the kinase Lck which phosphorylates proteins in the CD3 complex. This leads to phosphorylation of the adapter protein ZAP70 which then phosphorylates LAT and SLP76, recruiting downstream molecules. This results in calcium release, NFAT and NF-κB activation, and expression of cytokines and other proteins through similar pathways as in B cell signaling, including the Ras pathway. T cell signaling also regulates adhesion molecules and chemokines to influence T cell localization.
Fimmu 05-00055
This document discusses the role of dendritic cells (DCs) in autoimmune diseases. It begins by introducing DCs as professional antigen presenting cells that are involved in both inducing immune responses and maintaining peripheral tolerance. The review then examines the different DC subsets and their potential roles in tolerance induction. It discusses factors that influence the generation of tolerogenic DCs, including their maturation status, intrinsic characteristics, interactions with other immune cells, and the tissue microenvironment. The review challenges the traditional view that immature DCs induce tolerance, presenting evidence that both immature and mature DCs can induce tolerance depending on other factors. It highlights the need to better define the features of DC subsets that induce tolerance.
Manisha t cell
This document summarizes the key stages in T-cell maturation, activation, and differentiation. It discusses how T-cells mature in the thymus through positive and negative selection to screen for self-MHC restriction and eliminate self-reactive cells. Activation requires signal 1 through TCR-antigen-MHC interaction and signal 2 via co-stimulatory molecules. Upon activation, T-cells can proliferate and differentiate into memory cells or effector cells. CD4 and CD8 T-cells leave the thymus as naive cells and, upon antigen recognition, can become activated and further differentiate.
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Major Histocompatibility complex & Antigen Presentation and Processing
The document discusses the major histocompatibility complex (MHC) and antigen processing and presentation. It describes MHC molecules as polymorphic glycoproteins that play a role in discriminating self from non-self and participate in both humoral and cell-mediated immunity. MHC class I molecules present endogenous antigens on most nucleated cells and interact with CD8+ T cells. MHC class II molecules present exogenous antigens on antigen-presenting cells and interact with CD4+ T cells. Antigens are processed into peptides of appropriate size and bound motifs to be presented in the binding groove of MHC molecules.
B Cell Development
- B cell development begins with stem cells in the bone marrow, where they undergo a series of differentiation stages defined by immunoglobulin gene rearrangement under the influence of cytokines and contact with stromal cells.
- Successful rearrangement of the heavy and light chain genes leads to expression of a B cell receptor (BCR) and selection of clones that do not recognize self-antigens through deletion, anergy or receptor editing.
- Mature B cells that pass self-tolerance checkpoints are exported from the bone marrow to the peripheral immune system.
The T-Cell Antigen Receptor Complex
The document summarizes key points about the T-cell antigen receptor complex:
1) The T-cell receptor (TCR) is highly variable between individuals due to small changes in charge and shape at its ends, which allows it to recognize a diverse range of peptide antigens bound to MHC molecules.
2) TCR diversity is generated through combinatorial and junctional mechanisms similar to immunoglobulin genes, including the use of multiple variable, diversity and joining gene segments.
3) Unlike antibodies, TCRs do not undergo somatic mutation, which helps prevent autoimmunity by ensuring TCRs maintain recognition of peptide-MHC complexes.
T-Cell Mediated Immunity
T cells are activated through the recognition of antigen peptides presented on MHC complexes on antigen presenting cells (APCs). This leads to T cell proliferation and differentiation into effector T cells. Cytotoxic T cells recognize endogenous antigens on MHC I to kill infected cells, while helper T cells recognize exogenous peptides on MHC II and secrete cytokines to stimulate macrophage activation or B cell antibody production. Full T cell activation requires both antigen recognition by the TCR and co-stimulatory signaling between molecules such as B7 and CD28.
Antigens and immunogens immunogenecity
Immunogens are substances that can induce an immune response, while antigens are substances that can bind to antibodies or T-cell receptors. Not all antigens are immunogenic. The properties of an effective immunogen include foreignness, molecular size over 100,000 Daltons, chemical complexity, and the ability to be processed and presented by antigen-presenting cells. The immunogenicity of a substance depends on additional factors like dosage, route of administration, use of adjuvants, and host genetics. Antigens can be classified as exogenous, endogenous, autoantigens, or complete versus incomplete antigens.
T-cell activation
T-Cell Activation
• Concept of immune response
• T cell-mediated immune response
• B cell-mediated immune response
I. Concept of immune response
• A collective and coordinated response to the introduction of foreign substances in an individual mediated by the cells and molecules in the immune system.
II. T cell-mediated immune response
• Cell-mediated immunity is the arm of the adaptive immune response whose role is to combat infection of intracellular pathogens, such as intracellular bacteria (mycobacteria, listeria monocytogens), viruses, protozoa, etc.
Immunotolerance: mechanism and consequence
The document discusses several key mechanisms by which the immune system maintains tolerance to self-antigens to avoid autoimmunity. These include central tolerance in the thymus through negative selection which deletes self-reactive T cells, peripheral tolerance through ignorance, anergy, suppression and regulatory T cells, and the concept that tolerance is the default response unless danger signals are present to trigger an immune response. The timing of antigen exposure is also important, as antigens encountered during early development are more likely to induce tolerance.
Tumor immunology
This document discusses tumor immunology and cancer immunotherapy. It provides information on tumor antigens, how tumors stimulate an immune response, and mechanisms tumors use to evade the immune system. The document also outlines several approaches to cancer immunotherapy, including monoclonal antibodies, cytokines, and adoptive cell therapy. A brief history of cancer immunotherapy is given, noting early experiments in the 1890s using bacterial toxins to treat tumors and discoveries in the 1960s about antibody receptors and T cells recognizing cancer cells.
Tregs
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.
Mhc
The document discusses major histocompatibility complexes (MHCs), which are glycoproteins found on cell surfaces that present antigen fragments to T cells. It describes MHC Class I and Class II molecules, which present antigens from intracellular and extracellular pathogens, respectively. MHC genes were first identified as important in tissue graft rejection and show high polymorphism between individuals.
Tcr class
T-cell receptors are heterodimers consisting of alpha and beta chains with variable and constant regions. The variable region binds to antigens presented by the major histocompatibility complex and contains complementary determining regions that provide specificity. While the TCR is responsible for antigen recognition, it does not signal within the cell itself. Signal transduction is carried out by the CD3 complex, which contains gamma, delta, epsilon, and zeta chains and lacks kinase activity.
B cell Activation by T Independent & T Dependent Antigens-Dr C R Meera
During humoral immune response, Ab production is brought about by B lymphocytes. Based on the ability to induce Ab formation, antigens can be classified into T independent and T dependent antigens. Some antigens can directly induce the B cells to produce the Abs and are called T Independent Ans. However, some Ans require the help of T lymohocytes for the production of Abs from B cells. These Ans are called T Dependent Ans.
MHC and TCR
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.
Somatic hypermutation
Somatic hypermutation (SHM) introduces mutations in antibody genes in B cells, increasing antibody diversity and affinity for antigens. SHM occurs through the actions of activation-induced cytidine deaminase and other molecules at a rate of 10-3 mutations per base pair, compared to the typical spontaneous mutation rate of 10-8 per base pair. These mutations mainly occur in hypervariable regions of antibody genes and result from nucleotide substitutions. SHM leads to affinity maturation of B cells and increased antibody affinity for antigens. Future directions include using the SHM process to evolve proteins in mammalian cells.
Major Histocompatibility Complex
Some potential causes of the immune system attacking the self in autoimmune diseases include:
- Genetic predisposition - Genes coding for the variety of MHC molecules can influence susceptibility. A T cell's ability to respond is determined by MHC genotype. Differences in MHC alleles' ability to present autoantigens can play a role.
- Environmental triggers - Factors like infections, drugs, trauma, etc. may trigger autoimmunity in genetically susceptible individuals by molecular mimicry or other mechanisms.
- Loss of tolerance - Failure to eliminate self-reactive lymphocytes during development or maintain peripheral tolerance can allow self-reactivity.
- Hormonal factors - Many autoimmune diseases are more common in women and fluctuate with horm
MHC MOLECULES
The document discusses the major histocompatibility complex (MHC) in mammals. It notes that MHC acts as antigen presenting receptors and are involved in cell-cell interaction, antigen presentation, and recognition of self and non-self molecules. MHC is found on chromosome 6 in humans and is referred to as the HLA complex. MHC molecules are divided into three main classes - Class I MHC present antigens to cytotoxic T cells, Class II MHC present antigens to helper T cells, and Class III MHC genes encode complement components and cytokines. The structures and functions of Class I and Class II MHC molecules are described in detail.
Chapter 5 Immunology
T cells recognize antigens presented by MHC molecules on other cells. Antigens from intracellular sources such as viruses are processed and presented by MHC class I to CD8+ T cells. Antigens from extracellular sources such as bacteria that are endocytosed are processed and presented by MHC class II to CD4+ T cells. The antigen processing pathways and the classes of MHC molecules that present the peptides allow the immune system to mount appropriate responses targeting different types of pathogens.
Major histocompatibility complex
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.
Complement system
The document discusses the complement system of teleost fish. It has three pathways - the classical pathway, lectin pathway, and alternative pathway. All three pathways involve a cascade of complement components that ultimately lead to the formation of the membrane attack complex (MAC) on pathogen surfaces. The MAC forms pores that lyse pathogens. The complement system also opsonizes pathogens and generates inflammatory peptides like C3a and C5a. Strict regulation is needed to prevent damage to host cells, mediated by factors such as C1 inhibitor, factor H, decay accelerating factor, and CD59.
T cell signalling pathway
The T cell receptor signaling pathway involves T cells binding antigens presented by MHC proteins on antigen presenting cells. When the T cell receptor binds to its antigen, it activates the kinase Lck which phosphorylates proteins in the CD3 complex. This leads to phosphorylation of the adapter protein ZAP70 which then phosphorylates LAT and SLP76, recruiting downstream molecules. This results in calcium release, NFAT and NF-κB activation, and expression of cytokines and other proteins through similar pathways as in B cell signaling, including the Ras pathway. T cell signaling also regulates adhesion molecules and chemokines to influence T cell localization.
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This document discusses the role of dendritic cells (DCs) in autoimmune diseases. It begins by introducing DCs as professional antigen presenting cells that are involved in both inducing immune responses and maintaining peripheral tolerance. The review then examines the different DC subsets and their potential roles in tolerance induction. It discusses factors that influence the generation of tolerogenic DCs, including their maturation status, intrinsic characteristics, interactions with other immune cells, and the tissue microenvironment. The review challenges the traditional view that immature DCs induce tolerance, presenting evidence that both immature and mature DCs can induce tolerance depending on other factors. It highlights the need to better define the features of DC subsets that induce tolerance.
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This document summarizes the key stages in T-cell maturation, activation, and differentiation. It discusses how T-cells mature in the thymus through positive and negative selection to screen for self-MHC restriction and eliminate self-reactive cells. Activation requires signal 1 through TCR-antigen-MHC interaction and signal 2 via co-stimulatory molecules. Upon activation, T-cells can proliferate and differentiate into memory cells or effector cells. CD4 and CD8 T-cells leave the thymus as naive cells and, upon antigen recognition, can become activated and further differentiate.
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Proximity of TCR and its CD8 coreceptor controls sensitivity of T cells
a b s t r a c t
Spatial organisation of T cell receptor (TCR) and its coreceptor CD8 on the surface of live naïve and Ag-experienced CD8+ T cells was resolved by fluorescence lifetime cross-correlation microscopy. We found that exposure of naïve CD8+ T cells to antigen (Ag) causes formation of [TCR, CD8] functional ensembles on the cell surface which correlated with significantly enhanced sensitivity of these cells. In contrast, TCR and CD8 are randomly distributed on the surface of naïve cells. Our model suggests that close proximity of TCR and CD8 can increase Ag sensitivity of T cells by significant accelerating the TCR–peptide-major histocompatibility complex (pMHC) binding rate and stabilisation of this complex. We suggest that the proximity of these primary signalling molecules contributes to the mechanism of functional avidity maturation of CD8+ T cells by switching them from a low to high sensitivity mode. ©
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The subject deals with adoptive immunotherapy, introduction, its mechanism, processing and use of CAR-T cells, clinical trials and its efficacy. useful for oncology and newer advances in immunotherapy. Immunotherapy is treatment that uses a person's own immune system to fight cancer. Immunotherapy can boost or change how the immune system works so it can find and attack cancer cells. Cellular adoptive immunotherapy is a type of immunotherapy. Immune cells such as T-cells are usually isolated from patients for expansion or engineering purposes and reinfused back into patients to fight diseases using their own immune system.
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So, vaccines against infections and cancer considerably divided for prophylactic vaccines and therapeutic vaccines.
Anti Radiation Vaccine belonging to group vaccine which administered prophylactically.
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1
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MInh Project 2
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Pharm immuno9-11 portal
This document summarizes key concepts about cell-mediated immunity:
1. T cells recognize antigens presented by MHC molecules on antigen presenting cells and are activated, leading to clonal expansion and differentiation into effector T cells.
2. Effector T cells migrate to sites of infection where they carry out functions like activating macrophages to kill intracellular pathogens.
3. CD8+ T cells recognize antigens on infected cells and kill the infected cells through release of granzymes and perforin.
4. Cooperation between CD4+ and CD8+ T cells is needed to eliminate intracellular pathogens from infected cells and reservoirs.
CAR T CELL
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cdc42J Exp Med-2010-Pulecio-2719-32
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Immunological Abnormalities in Liver Carcinoma
1) Hepatocellular carcinoma (HCC) has a poor prognosis and limited treatment options. While immune therapies show promise, the response of HCC has been unsatisfactory due to its immunosuppressive microenvironment.
2) Dendritic cells activate T cells to target cancer cells, but in HCC various immune cells and cytokines like regulatory T cells and TGF-β promote immune suppression.
3) Future therapies aim to modulate this microenvironment through vaccines, adoptive cell transfer, immune checkpoint blockade, and other approaches to achieve effective anti-tumor immunity against HCC.
Immunology
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IDO pathway from bench to clinic
This document outlines the history and mechanisms of the indoleamine-2,3-dioxygenase (IDO) pathway and its role in cancer immunotherapy. It discusses key findings such as:
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4) Ongoing clinical
Stat3 protein & t helper 17 cell -in psoriasis by yousry a mawla
This document discusses the roles of STAT3 and Th17 cells in psoriasis. STAT3 is activated by cytokines like IL-6 and transduces signals that lead to the transcription of genes involved in inflammation. Th17 cells secrete IL-17 which stimulates keratinocytes and drives the inflammatory response in psoriasis. The immune cells and cytokines involved create a vicious cycle that perpetuates the chronic inflammation and characteristic lesions of the disease.
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Proximity of TCR and its CD8 coreceptor controls sensitivity of T cells
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Immunological synapse
- 1. IMMUNOLOGICAL SYNAPSE Presented by Candice Churaman Charles Okonkwo Shawn Felix
- 2. An immunological synapse also known as a supramolecular adhesion complex (SMAC) is the cell to cell contact between the T cell, its co-receptors and the antigen presenting cell.
- 3. The site of contact is composed of concentric rings with each containing segregated cluster of proteins : Central supramolecular activation complex (cSMAC) - comprises of the T cell receptor, it’s co-receptor (CD 4 or CD 8), CD 28, CD 2 and PKC θ
- 4. Peripheral supramolecular activation complex (pSMAC) - comprises of LFA1, ICAM-1 and talin Distal supramolecular activation complex (dSMAC) - enriched in CD 43, CD44 and CD 45
- 5. Enhancing signalling Terminating signalling and/or effector function Balancing signalling Directing secretion
- 6. • The mechanism of immune synapse are: passive and active. • Passive is defined as: binding and steric factors. (Čemerski and Shaw, 2006) The diagram on the left shows the mechanisms of redistribution and segregation of molecules at the cell surface. Fig.1: The mechanisms involved in synapse formation. (Čemerski and Shaw, 2006)
- 7. Active Mechanism: This is the lateral movement on the surface and polarised exocytosis of vesicular stores. (van der Merwe et al., 2000) There are various amounts of cell surface molecules which is transported from the intracellular vesicular compartments to the immune synapse. Examples of these are: FasL & CTLA-4. (van der Merwe et al., 2000) Fig.2: The transportation of cell surface molecules into the intracellular vesicular compartments. (van der Merwe et al., 2000)
- 8. IMMUNOLOGICAL SYNAPSE- Pathology : HIV as a case study Model of virological and immunological synapse formation in the contribution to HIV persistence Virological synapse (left panel) is mediated through interactions of gp41/gp1209(shown in red) on an HIV-infected CD4+T cell with CD4+ (brown) on the cell surface of an uninfected target CD4+ T cell. Interactions are stabilized by ICAM-1(green) and LFA-1(blue) and takes place even in the presence of ART. IS formation(right panel) initiated through interaction of MHC class II(green) on an APC and the TCR(red) of an Infected T cell may induce latency via inhibitory signals within the IS to reduce T-cell activation.
- 9. Trends in Immunological synapse Then Shows the contact region between T-cells and APCs that forms upon TCR stimulation with peptide – MHC In addition to naïve and effector T cells, also found in other immune system cells. Example: CTLs, NK cells, NKTcells and B cells A concentric bull’s eye structure consisting of 3 sub regions: cSMAC, pSMAC and DPC. Now TCR microclusters(MCs) containing additional signalling molecules defined as the minimal active signalling unit of IS Existence of kinapses, short lived asymmetric synapses, in motile T cells. Segregation of the cSMAC into two distinct sub regions – a central, CD3high region(signal termination) and an outer CD3low annular ring enriched in CD28 and PKCθ,a site of sustained signalling.
- 10. Conclusion IS involves reorganization of not only cell surface receptors, but also actin and microtubule cytoskeletons leading to signalling and secretion Further work elucidating a clear pathway that regulates centrosome movement within immune cells is still required. References : J.C. Stinchcombe, G.M. Griffiths. The role of the secretory immunological synapse in killing by CD8+ CTL. Semin. Immunol., 15 (2003), pp. 301–305 Colin L., Van Lint C. Molecular control of HIV-1 postintegration latency: implications for the development of new therapeutic strategies. Retrovirology. 2009; 6:111. PubMed.
- 11. Angus, K. and Griffiths, G. (2013). Cell polarisation and the immunological synapse. Current Opinion in Cell Biology, 25(1), pp.85-91. Čemerski, S. and Shaw, A. (2006). Immune synapses in T-cell activation. Current Opinion in Immunology, 18(3), pp.298-304. Davis, D. and Dustin, M. (2004). What is the importance of the immunological synapse?. Trends in Immunology, 25(6), pp.323-327. Rodríguez-Fernández, J., Riol-Blanco, L. and Delgado-Martín, C. (2010). What is an immunological synapse?. Microbes and Infection, 12(6), pp.438-445.
- 12. Van der Merwe, P. (2002). Formation and function of the immunological synapse. Current Opinion in Immunology, 14(3), pp.293-298. Van der Merwe, P., Davis, S., Shaw, A. and Dustin, M. (2000). Cytoskeletal polarization and redistribution of cell-surface molecules during T cell antigen recognition. Seminars in Immunology, 12(1), pp.5-21.