HIV primarily infects CD4+ T-cells, establishing chronic immune activation that allows the virus to thrive. During infection, HIV uses error-prone reverse transcription to establish latent reservoirs within the host. This makes eradication of the virus difficult as it develops escape mutants to evade both humoral immunity through antibody neutralization and cellular immunity from CD8+ T cells. While monocytes, macrophages, dendritic cells and natural killer cells are less affected numerically, they show functional deficiencies that allow persistence and spread of the infection throughout the immune system.
This document summarizes the immune response to HIV infection. It discusses how CD4 T-cells, cytotoxic T-cells, B-cells, and antigen presenting cells respond to HIV. Cytotoxic T-cells target many HIV proteins but often cannot eliminate the virus due to epitope escape, exhaustion, or suboptimal responses. Antibody responses have difficulty neutralizing HIV due to properties of the gp120 and gp41 envelope proteins. The immune response ultimately fails to clear HIV because the virus can integrate into genes, mutate, and impair antigen presenting cell function.
Immune response during bacterial, parasitic and viral infection.pptxVanshikaVarshney5
1) The innate immune response to viruses involves interferon production which stimulates antiviral proteins to block viral replication. Natural killer cells also help destroy infected cells.
2) The adaptive immune response involves humoral immunity with antiviral antibodies that neutralize viruses and prevent infection of cells. Cell-mediated immunity uses cytotoxic T-cells and macrophages to directly kill infected cells.
3) Viruses have evolved mechanisms to evade the immune response, such as reducing MHC expression to avoid detection by T-cells, direct immunosuppression, and antigenic variation for influenza virus.
This document discusses immunological tolerance and regulatory T cells. It defines tolerance as unresponsiveness to antigen induced by previous exposure. Central tolerance occurs in the thymus through deletion of self-reactive T cells. Peripheral tolerance occurs through several mechanisms in tissues, including regulatory T cells that suppress immune responses. The key transcription factor controlling regulatory T cells is FOXP3. Mutations in FOXP3 can lead to immune dysregulation diseases like IPEX syndrome.
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.
Mechanism of immunoevasion in parasites 2018 06-17Rasika Deshmukh
The document summarizes mechanisms of immune evasion in various parasites. It discusses how parasites like malaria, trypanosomes, leishmania, toxoplasma, entamoeba, giardia, schistosomes, trichomonas, and helminths evade the host immune system. Some key strategies parasites use include antigenic disguise, molecular mimicry, immunosuppression through cytokines, inhibiting host immune signaling pathways, disrupting complement pathways, shedding surface antigens, and phenotypic variation. Understanding these immune evasion mechanisms provides insights into host-parasite interactions and disease pathogenesis.
HIV primarily infects CD4+ T-cells, establishing chronic immune activation that allows the virus to thrive. During infection, HIV uses error-prone reverse transcription to establish latent reservoirs within the host. This makes eradication of the virus difficult as it develops escape mutants to evade both humoral immunity through antibody neutralization and cellular immunity from CD8+ T cells. While monocytes, macrophages, dendritic cells and natural killer cells are less affected numerically, they show functional deficiencies that allow persistence and spread of the infection throughout the immune system.
This document summarizes the immune response to HIV infection. It discusses how CD4 T-cells, cytotoxic T-cells, B-cells, and antigen presenting cells respond to HIV. Cytotoxic T-cells target many HIV proteins but often cannot eliminate the virus due to epitope escape, exhaustion, or suboptimal responses. Antibody responses have difficulty neutralizing HIV due to properties of the gp120 and gp41 envelope proteins. The immune response ultimately fails to clear HIV because the virus can integrate into genes, mutate, and impair antigen presenting cell function.
Immune response during bacterial, parasitic and viral infection.pptxVanshikaVarshney5
1) The innate immune response to viruses involves interferon production which stimulates antiviral proteins to block viral replication. Natural killer cells also help destroy infected cells.
2) The adaptive immune response involves humoral immunity with antiviral antibodies that neutralize viruses and prevent infection of cells. Cell-mediated immunity uses cytotoxic T-cells and macrophages to directly kill infected cells.
3) Viruses have evolved mechanisms to evade the immune response, such as reducing MHC expression to avoid detection by T-cells, direct immunosuppression, and antigenic variation for influenza virus.
This document discusses immunological tolerance and regulatory T cells. It defines tolerance as unresponsiveness to antigen induced by previous exposure. Central tolerance occurs in the thymus through deletion of self-reactive T cells. Peripheral tolerance occurs through several mechanisms in tissues, including regulatory T cells that suppress immune responses. The key transcription factor controlling regulatory T cells is FOXP3. Mutations in FOXP3 can lead to immune dysregulation diseases like IPEX syndrome.
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.
Mechanism of immunoevasion in parasites 2018 06-17Rasika Deshmukh
The document summarizes mechanisms of immune evasion in various parasites. It discusses how parasites like malaria, trypanosomes, leishmania, toxoplasma, entamoeba, giardia, schistosomes, trichomonas, and helminths evade the host immune system. Some key strategies parasites use include antigenic disguise, molecular mimicry, immunosuppression through cytokines, inhibiting host immune signaling pathways, disrupting complement pathways, shedding surface antigens, and phenotypic variation. Understanding these immune evasion mechanisms provides insights into host-parasite interactions and disease pathogenesis.
This document provides an overview of autoimmune diseases. It discusses how a defect in the immune system can trigger autoimmunity and lists examples of autoimmune disorders like rheumatoid arthritis, Graves' disease, and Hashimoto's thyroiditis. The causes of autoimmunity include genetic susceptibility and environmental triggers like infections. Viruses can induce autoimmunity through molecular mimicry or by damaging tissues and exposing new antigens.
This document summarizes cellular immune response (CMI) mediated by sensitized T cells. It describes how CMI is induced through antigen presentation and T cell receptor binding, leading to T cell proliferation and differentiation. The two main effector mechanisms of CMI are the release of cytokines like interleukin-2 and tumor necrosis factor, and the generation of cytotoxic T cells. Cytokines regulate immune cells and have various metabolic and inflammatory effects. Cytotoxic T cells directly kill target cells like virus-infected cells. Tests to detect CMI include skin tests and lymphocyte transformation assays in vitro. CMI plays an important role in immunity against intracellular pathogens and transplants.
The document discusses bacterial pathogenesis and virulence. It describes three main ways bacteria cause disease: 1) invasiveness through mechanisms like adhesion and toxin production, 2) toxigenesis through exotoxins and endotoxins, and 3) evading host immune responses. Specific virulence factors and pathogenesis mechanisms are discussed for different bacteria like Pseudomonas aeruginosa and Mycobacterium tuberculosis. The host barriers bacteria must overcome include phagocytosis, complement activation, and adaptive immune responses; bacteria have evolved strategies to inhibit or subvert these defenses.
1. Innate immunity provides the first line of defense against pathogens and includes anatomical barriers, inflammation, phagocytosis, and antimicrobial proteins/peptides.
2. Adaptive immunity develops over time upon exposure to specific pathogens and provides enhanced protection through antibody production and immunological memory.
3. The major categories of innate immunity defenses are anatomical barriers, inflammation, phagocytosis, microbial antagonism by normal flora, and antimicrobial substances in tissues. Adaptive immunity involves B cells, T cells, and production of antibodies.
This document summarizes fungal infections and the immune response against fungi. It discusses that fungi are recognized by immune cells through pattern recognition receptors which activate downstream responses like phagocytosis and adaptive immunity like Th1 and Th17 cells. However, fungi have developed mechanisms to evade the immune system like modifying their cell wall to avoid detection and utilizing host nutrients like iron. An effective vaccine is still needed as current antifungal drugs are only partially successful in treating invasive fungal infections.
The document discusses immunological tolerance and its breakdown which can lead to autoimmunity and autoimmune diseases. It explains the mechanisms of central and peripheral tolerance that normally prevent immune responses against self-antigens. Failure of these tolerance mechanisms can occur through various causes like a breakdown of T cell anergy or loss of regulatory T cells, resulting in an immune response against self-tissues and the development of autoimmune conditions.
Primary immunodeficiencies are present at birth and can affect adaptive or innate immune functions. The most common secondary immunodeficiency is acquired immunodeficiency syndrome (AIDS), which is caused by the human immunodeficiency virus (HIV-1). HIV-1 infects and kills CD4+ T cells, eventually leaving the body vulnerable to opportunistic infections. While antiretroviral drugs can suppress HIV-1 and prolong life, developing an effective vaccine remains the best option to prevent the spread of AIDS.
Cytokines are low molecular weight polypeptides or glycoproteins that are secreted by cells and have various functions including mediating and regulating immune responses and inflammatory reactions. Cytokines are produced by lymphocytes, monocytes, macrophages, mast cells, glial cells and other cells. They act through autocrine, paracrine or endocrine mechanisms and initiate their actions by binding to specific membrane receptors. Cytokines have pleiotropic, redundant, synergistic and antagonistic effects and form a cytokine network. The major classes of cytokines include interleukins, tumor necrosis factors, interferons, colony stimulating factors, transforming growth factors and chemokines. Cytokines play important roles in various diseases and their therapeutic uses include treatment
Major Histocompatibility complex & Antigen Presentation and ProcessingSreeraj Thamban
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.
Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism. Immune tolerance is important for normal physiology. Central tolerance is the main way the immune system learns to discriminate self from non-self. Peripheral tolerance is key to preventing over-reactivity of the immune system to various environmental entities (allergens, gut microbes, etc.).
This document summarizes immunity to fungal infections. It discusses that fungi are diverse organisms that can cause opportunistic infections in immunocompromised individuals. Innate immunity provides the first line of defense through physical barriers and immune cells like neutrophils and macrophages. Adaptive immunity involves both humoral responses and cell-mediated responses through T cells. Dendritic cells link the innate and adaptive responses by phagocytosing fungi and presenting antigens to T cells. Cytokines released by immune cells control the Th1/Th2 response. Fungi have developed mechanisms to evade the immune response. Vaccines against some dermatophytic fungi have been developed.
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.
The document discusses the theory of immune surveillance, which proposes that the immune system patrols the body to recognize and destroy both invading pathogens and abnormal host cells, such as cancer cells. It provides evidence from experiments in mice and clinical observations in humans that support this theory. The key components of immune surveillance systems that eliminate cancer cells are natural killer cells, cytotoxic T-lymphocytes, B-cells and macrophages. The process by which cancer cells can evade immune destruction is called immunoediting, which occurs through three sequential phases - elimination, equilibrium, and escape.
1. Immune tolerance occurs when the immune system fails to respond to an antigen it has previously been exposed to, resulting in non-reactivity to that antigen. Tolerance is important for avoiding autoimmune reactions to self-antigens.
2. Tolerance can occur through several mechanisms, including clonal deletion of autoreactive T and B cells in the thymus and bone marrow, clonal anergy of autoreactive cells, ignorance of sequestered self-antigens, and receptor editing of B cells.
3. Autoimmunity results from a loss of self-tolerance and an immune response against self-components. It can be organ-specific or systemic. Causes of autoimmunity
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
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.
immunology chapter 9 : activation of T lymphocytesprincesa_mera
1. T lymphocyte activation involves recognition of antigen peptides presented by MHC molecules on antigen presenting cells. This provides an initial activation signal that is enhanced by costimulatory molecules like B7 and CD28.
2. Upon activation, naive T cells proliferate extensively through clonal expansion, increasing the number of antigen-specific T cells by 100,000-fold. They also differentiate into effector T cell subsets.
3. The main effector T cell subsets are TH1 and TH2 cells, distinguished by their cytokine production. TH1 cells produce IFNγ and activate macrophages, while TH2 cells produce IL-4 and stimulate antibody class switching and eosinophil responses.
T-cells are a type of white blood cell that play a major role in the immune system by fighting infection. There are different types of T-cells that act in various ways to identify and destroy pathogens. T-cells mature and develop in the thymus gland, where they are selected and educated to recognize the body's own cells and mount immune responses against foreign threats. T-cells recognize antigens presented on other cells through molecules of the major histocompatibility complex and are activated through a process that involves antigen presentation, costimulatory signals, and cytokine communication.
This document discusses immunosurveillance and immunotherapy for cancer treatment. It explains that the immune system normally surveils and destroys mutated cells to prevent tumor development, but tumors can evade this response through various mechanisms such as antigen shedding or fast proliferation. Immunotherapy aims to boost the immune system's ability to fight cancer, for example through monoclonal antibodies, non-specific stimulants, cancer vaccines, or T-cell therapies.
This document summarizes information about HIV/AIDS. It begins by noting that the first reported HIV case was in 1981 and the virus was isolated in 1983. There are two types of HIV - HIV-1 and HIV-2. HIV is believed to have originated from closely related viruses found in non-human primates. The virus is transmitted primarily through unprotected sexual intercourse and contaminated blood/needles. While antiretroviral therapy has slowed the pandemic, there is still no cure for HIV/AIDS. The document outlines the pathogenesis, clinical stages, diagnosis, and transmission routes of HIV in further detail over multiple pages.
The document discusses the immunology of tuberculosis. It covers the stages of pathogenesis of M. tuberculosis infection, the host immune response including innate and acquired immunity, and the pro-inflammatory and anti-inflammatory mediators involved in tuberculosis. The key points are:
1) M. tuberculosis is an intracellular pathogen that infects the lungs and can spread to other organs. The host immune response involves phagocytosis by alveolar macrophages and recruitment of other immune cells.
2) Both the innate and acquired immune responses are involved in the host defense against M. tuberculosis. Important components include neutrophils, NK cells, TLR signaling, and the cell-mediated immune response involving CD4 and CD8 T cells.
This document provides an overview of autoimmune diseases. It discusses how a defect in the immune system can trigger autoimmunity and lists examples of autoimmune disorders like rheumatoid arthritis, Graves' disease, and Hashimoto's thyroiditis. The causes of autoimmunity include genetic susceptibility and environmental triggers like infections. Viruses can induce autoimmunity through molecular mimicry or by damaging tissues and exposing new antigens.
This document summarizes cellular immune response (CMI) mediated by sensitized T cells. It describes how CMI is induced through antigen presentation and T cell receptor binding, leading to T cell proliferation and differentiation. The two main effector mechanisms of CMI are the release of cytokines like interleukin-2 and tumor necrosis factor, and the generation of cytotoxic T cells. Cytokines regulate immune cells and have various metabolic and inflammatory effects. Cytotoxic T cells directly kill target cells like virus-infected cells. Tests to detect CMI include skin tests and lymphocyte transformation assays in vitro. CMI plays an important role in immunity against intracellular pathogens and transplants.
The document discusses bacterial pathogenesis and virulence. It describes three main ways bacteria cause disease: 1) invasiveness through mechanisms like adhesion and toxin production, 2) toxigenesis through exotoxins and endotoxins, and 3) evading host immune responses. Specific virulence factors and pathogenesis mechanisms are discussed for different bacteria like Pseudomonas aeruginosa and Mycobacterium tuberculosis. The host barriers bacteria must overcome include phagocytosis, complement activation, and adaptive immune responses; bacteria have evolved strategies to inhibit or subvert these defenses.
1. Innate immunity provides the first line of defense against pathogens and includes anatomical barriers, inflammation, phagocytosis, and antimicrobial proteins/peptides.
2. Adaptive immunity develops over time upon exposure to specific pathogens and provides enhanced protection through antibody production and immunological memory.
3. The major categories of innate immunity defenses are anatomical barriers, inflammation, phagocytosis, microbial antagonism by normal flora, and antimicrobial substances in tissues. Adaptive immunity involves B cells, T cells, and production of antibodies.
This document summarizes fungal infections and the immune response against fungi. It discusses that fungi are recognized by immune cells through pattern recognition receptors which activate downstream responses like phagocytosis and adaptive immunity like Th1 and Th17 cells. However, fungi have developed mechanisms to evade the immune system like modifying their cell wall to avoid detection and utilizing host nutrients like iron. An effective vaccine is still needed as current antifungal drugs are only partially successful in treating invasive fungal infections.
The document discusses immunological tolerance and its breakdown which can lead to autoimmunity and autoimmune diseases. It explains the mechanisms of central and peripheral tolerance that normally prevent immune responses against self-antigens. Failure of these tolerance mechanisms can occur through various causes like a breakdown of T cell anergy or loss of regulatory T cells, resulting in an immune response against self-tissues and the development of autoimmune conditions.
Primary immunodeficiencies are present at birth and can affect adaptive or innate immune functions. The most common secondary immunodeficiency is acquired immunodeficiency syndrome (AIDS), which is caused by the human immunodeficiency virus (HIV-1). HIV-1 infects and kills CD4+ T cells, eventually leaving the body vulnerable to opportunistic infections. While antiretroviral drugs can suppress HIV-1 and prolong life, developing an effective vaccine remains the best option to prevent the spread of AIDS.
Cytokines are low molecular weight polypeptides or glycoproteins that are secreted by cells and have various functions including mediating and regulating immune responses and inflammatory reactions. Cytokines are produced by lymphocytes, monocytes, macrophages, mast cells, glial cells and other cells. They act through autocrine, paracrine or endocrine mechanisms and initiate their actions by binding to specific membrane receptors. Cytokines have pleiotropic, redundant, synergistic and antagonistic effects and form a cytokine network. The major classes of cytokines include interleukins, tumor necrosis factors, interferons, colony stimulating factors, transforming growth factors and chemokines. Cytokines play important roles in various diseases and their therapeutic uses include treatment
Major Histocompatibility complex & Antigen Presentation and ProcessingSreeraj Thamban
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.
Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism. Immune tolerance is important for normal physiology. Central tolerance is the main way the immune system learns to discriminate self from non-self. Peripheral tolerance is key to preventing over-reactivity of the immune system to various environmental entities (allergens, gut microbes, etc.).
This document summarizes immunity to fungal infections. It discusses that fungi are diverse organisms that can cause opportunistic infections in immunocompromised individuals. Innate immunity provides the first line of defense through physical barriers and immune cells like neutrophils and macrophages. Adaptive immunity involves both humoral responses and cell-mediated responses through T cells. Dendritic cells link the innate and adaptive responses by phagocytosing fungi and presenting antigens to T cells. Cytokines released by immune cells control the Th1/Th2 response. Fungi have developed mechanisms to evade the immune response. Vaccines against some dermatophytic fungi have been developed.
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.
The document discusses the theory of immune surveillance, which proposes that the immune system patrols the body to recognize and destroy both invading pathogens and abnormal host cells, such as cancer cells. It provides evidence from experiments in mice and clinical observations in humans that support this theory. The key components of immune surveillance systems that eliminate cancer cells are natural killer cells, cytotoxic T-lymphocytes, B-cells and macrophages. The process by which cancer cells can evade immune destruction is called immunoediting, which occurs through three sequential phases - elimination, equilibrium, and escape.
1. Immune tolerance occurs when the immune system fails to respond to an antigen it has previously been exposed to, resulting in non-reactivity to that antigen. Tolerance is important for avoiding autoimmune reactions to self-antigens.
2. Tolerance can occur through several mechanisms, including clonal deletion of autoreactive T and B cells in the thymus and bone marrow, clonal anergy of autoreactive cells, ignorance of sequestered self-antigens, and receptor editing of B cells.
3. Autoimmunity results from a loss of self-tolerance and an immune response against self-components. It can be organ-specific or systemic. Causes of autoimmunity
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
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.
immunology chapter 9 : activation of T lymphocytesprincesa_mera
1. T lymphocyte activation involves recognition of antigen peptides presented by MHC molecules on antigen presenting cells. This provides an initial activation signal that is enhanced by costimulatory molecules like B7 and CD28.
2. Upon activation, naive T cells proliferate extensively through clonal expansion, increasing the number of antigen-specific T cells by 100,000-fold. They also differentiate into effector T cell subsets.
3. The main effector T cell subsets are TH1 and TH2 cells, distinguished by their cytokine production. TH1 cells produce IFNγ and activate macrophages, while TH2 cells produce IL-4 and stimulate antibody class switching and eosinophil responses.
T-cells are a type of white blood cell that play a major role in the immune system by fighting infection. There are different types of T-cells that act in various ways to identify and destroy pathogens. T-cells mature and develop in the thymus gland, where they are selected and educated to recognize the body's own cells and mount immune responses against foreign threats. T-cells recognize antigens presented on other cells through molecules of the major histocompatibility complex and are activated through a process that involves antigen presentation, costimulatory signals, and cytokine communication.
This document discusses immunosurveillance and immunotherapy for cancer treatment. It explains that the immune system normally surveils and destroys mutated cells to prevent tumor development, but tumors can evade this response through various mechanisms such as antigen shedding or fast proliferation. Immunotherapy aims to boost the immune system's ability to fight cancer, for example through monoclonal antibodies, non-specific stimulants, cancer vaccines, or T-cell therapies.
This document summarizes information about HIV/AIDS. It begins by noting that the first reported HIV case was in 1981 and the virus was isolated in 1983. There are two types of HIV - HIV-1 and HIV-2. HIV is believed to have originated from closely related viruses found in non-human primates. The virus is transmitted primarily through unprotected sexual intercourse and contaminated blood/needles. While antiretroviral therapy has slowed the pandemic, there is still no cure for HIV/AIDS. The document outlines the pathogenesis, clinical stages, diagnosis, and transmission routes of HIV in further detail over multiple pages.
The document discusses the immunology of tuberculosis. It covers the stages of pathogenesis of M. tuberculosis infection, the host immune response including innate and acquired immunity, and the pro-inflammatory and anti-inflammatory mediators involved in tuberculosis. The key points are:
1) M. tuberculosis is an intracellular pathogen that infects the lungs and can spread to other organs. The host immune response involves phagocytosis by alveolar macrophages and recruitment of other immune cells.
2) Both the innate and acquired immune responses are involved in the host defense against M. tuberculosis. Important components include neutrophils, NK cells, TLR signaling, and the cell-mediated immune response involving CD4 and CD8 T cells.
The document summarizes antigen processing and presentation by cells. It describes how T lymphocytes recognize short peptide antigens displayed by MHC molecules on antigen-presenting cells. Dendritic cells are specialized to capture antigens through receptors and transport them to lymph nodes for presentation to T cells. Proteins are broken down by proteasomes and cathepsins into peptides that bind MHC class I and class II, respectively, for recognition by CD8+ and CD4+ T cells.
This document discusses transplantation and hematopoietic stem cell transplantation (HSCT). It defines different types of transplantation and describes adaptive immune responses to allografts. It also discusses graft rejection, complications of HSCT like graft-versus-host disease, and the use of HSCT to treat primary immunodeficiency disorders like severe combined immunodeficiency (SCID). Factors that influence survival and quality of immune reconstitution after HSCT for SCID are also summarized.
The document outlines the immune response to viral infections. It discusses that viruses are obligate intracellular parasites that cannot replicate without hijacking a host cell. The innate immune response includes epithelial barriers, interferons like IFN-α and IFN-β, natural killer cells, and macrophages. Adaptive responses involve antiviral antibodies that can neutralize viruses or mediate antibody-dependent cellular cytotoxicity, as well as cytotoxic T lymphocytes that identify and kill infected cells. Overall, the immune system employs diverse innate and adaptive mechanisms to recognize, control and clear viral infections.
This document discusses the history and mechanisms of immunosuppressant drugs. It begins by outlining the early development of corticosteroids and other drugs in the 1940s-1970s to prevent organ transplant rejection. It then details several classes of immunosuppressants based on their molecular targets and cellular effects, including monoclonal antibodies, T cell-directed agents like calcineurin inhibitors, B cell-directed agents like Rituximab, agents targeting cytokines and chemokines, and non-specific pan-lymphocyte depleting agents. For each drug class and example drug, it describes the relevant immune cells and pathways that are modulated to achieve 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.
This document provides information about HIV/AIDS, including:
- It defines endemic, epidemic, and pandemic, with AIDS classified as a pandemic.
- As of 2003, it was estimated that 40 million people worldwide were living with HIV/AIDS, with 25-28.2 million in Sub-Saharan Africa.
- HIV attacks and destroys CD4 cells, weakening the immune system and leaving the body vulnerable to opportunistic infections over time without treatment.
- HIV is transmitted through direct contact with infected bodily fluids like blood, semen, vaginal fluids. It cannot be transmitted by casual contact.
- Prevention strategies include blood screening, education on safer sex practices, STI treatment, and preventing mother
Protozoan parasites cause diseases like malaria, leishmaniasis, and trypanosomiasis. Both the innate and adaptive immune systems play crucial roles in defending against protozoan infections. The innate immune system includes mechanisms like cytokines, complement proteins, macrophages, and neutrophils. The adaptive immune system involves antibody production and T cell responses. Protozoan parasites have evolved ways to evade or subvert the host immune response, such as antigenic variation and inhibiting immune cell function, enabling chronic or recurrent infections. An effective immune response against protozoa involves a balance of pro-inflammatory cytokines, T cell subsets, and effector cells and molecules.
This document discusses Type IV hypersensitivity reactions, which are mediated by T cells. It describes how CD4+ T cells can differentiate into Th1 and Th17 effector cells that promote inflammation through cytokine production. It also explains the three pathways through which CD8+ T cells exert their cytotoxic effects: cytotoxin mediated killing, Fas-mediated apoptosis, and cytokine production. Finally, it provides several clinical examples of conditions involving CD4+ and CD8+ T cell-mediated hypersensitivity, such as tuberculosis and autoimmune diseases.
As a periodontist, I have included the basics of immunity from the periodontist point of view that will help in understanding the immunological basis of periodontal disease...
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.
Immune responses in periodontal disease final.pptxmalti19
This document discusses the immune responses involved in periodontal disease. It begins by defining periodontitis as an infectious disease caused by anaerobic bacteria. Both bacteria and a susceptible host are required to cause disease. It then describes the pathogenesis which involves environmental and genetic risk factors interacting with the microbial challenge to activate the host immune response, resulting in inflammation and bone/tissue destruction. The document discusses the types of immunity, including innate and adaptive immunity. It covers topics such as dendritic cells, T-cell and B-cell roles, the roles of cytokines and RANKL in linking the immune response to bone loss, and hypotheses about the roles of the Th1 and Th2 responses in periodontitis.
This document provides an overview of the immune system and how it responds to microbial infections. It discusses both the innate and adaptive immune responses. The innate response involves inflammation, complement activation, NK cells, and activation of antigen presenting cells. The adaptive response involves activation of naive T lymphocytes, polarization of T cells into Th1 and Th2 subsets, roles of Th1 and Th2 cells, and roles of memory B and T cells in providing long-term protective immunity. The document also briefly discusses some methods microbes use to evade the immune system.
The document discusses diseases of immunity, including hypersensitivity reactions and autoimmune diseases. It describes the innate and adaptive immune system, cells involved like T cells, B cells, cytokines, and histocompatibility molecules. Hypersensitivity reactions are classified and immediate (Type I) hypersensitivity is explained, where re-exposure to an antigen leads to rapid allergic reactions mediated by IgE and mast cells.
The document discusses diseases of immunity, including hypersensitivity reactions and autoimmune diseases. It describes the innate and adaptive immune system, cells involved like T cells, B cells, cytokines, and histocompatibility molecules. Hypersensitivity reactions are classified and immediate (Type I) hypersensitivity is explained, where re-exposure to an antigen leads to rapid allergic reactions mediated by IgE and mast cells.
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
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.
Evaluation and importance of innate & adaptive immunity Dr. ihsan edan ab...dr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
The document discusses the immune system, including both innate and adaptive immunity. It provides details on the components and functions of the innate immune system, such as physical barriers, white blood cells, and cytokines. Adaptive immunity involves lymphocytes and develops a specific response along with memory. The adaptive response includes both humoral immunity carried out by B cells and antibodies, as well as cell-mediated immunity involving T cells. Key aspects covered are antigen presentation, roles of T cell subsets, and the relationship between the humoral and cell-mediated responses.
The document provides an overview of the immune system, including:
1. It differentiates between innate and adaptive immunity and describes cells involved in each.
2. It outlines the properties of adaptive immunity including specificity and memory.
3. It describes the tissues and organs of the immune system including peripheral lymphoid organs and lymphocyte circulation.
This document provides an overview of basic immunology. It begins with an introduction to immunity, the immune system, and immunology. It then discusses the history of immunology, types of immunity including innate and acquired immunity. It describes the tissues and cells involved in immunity. It covers basic aspects like antigens, antibodies, antigen-antibody reactions, and the complement system. It also discusses major histocompatibility complex, cytokines, immune disorders, and immune responses in periodontal pathogenesis.
Immune response to infectious agents.pptxahmed811332
This document provides an overview of immune responses to infectious agents. It begins by distinguishing innate and adaptive immunity. Innate immunity consists of nonspecific defenses like physical barriers and phagocytosis. Adaptive immunity is acquired through antigen exposure and leads to immunological memory. The document then covers specific innate immune cells and molecules like TLRs and the inflammatory response. It discusses adaptive immunity including B and T cells. Finally, it applies these concepts to examples of viral, bacterial, parasitic and fungal infections.
Describes the basic properties and mechanisms of T cells and B cells in maintaining Immune Response against foreign antigens or infections and covers the UG and PG portion of immunology.
Innate and adaptive immunity work together to defend the body. Innate immunity provides immediate defense through physical barriers and cells that recognize pathogens. Adaptive immunity develops over time and mounts targeted responses through immunoglobulins and T cells with memory. Understanding these systems is fundamental to immunology and its role in disease pathology, diagnosis, and treatment. Key cells involved include macrophages, neutrophils, dendritic cells, T and B cells, which communicate through cytokines, interferons and chemokines to mount inflammatory or specialized immune responses.
This presentation explores a brief idea about the structural and functional attributes of nucleotides, the structure and function of genetic materials along with the impact of UV rays and pH upon them.
The debris of the ‘last major merger’ is dynamically youngSérgio Sacani
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
The use of Nauplii and metanauplii artemia in aquaculture (brine shrimp).pptxMAGOTI ERNEST
Although Artemia has been known to man for centuries, its use as a food for the culture of larval organisms apparently began only in the 1930s, when several investigators found that it made an excellent food for newly hatched fish larvae (Litvinenko et al., 2023). As aquaculture developed in the 1960s and ‘70s, the use of Artemia also became more widespread, due both to its convenience and to its nutritional value for larval organisms (Arenas-Pardo et al., 2024). The fact that Artemia dormant cysts can be stored for long periods in cans, and then used as an off-the-shelf food requiring only 24 h of incubation makes them the most convenient, least labor-intensive, live food available for aquaculture (Sorgeloos & Roubach, 2021). The nutritional value of Artemia, especially for marine organisms, is not constant, but varies both geographically and temporally. During the last decade, however, both the causes of Artemia nutritional variability and methods to improve poorquality Artemia have been identified (Loufi et al., 2024).
Brine shrimp (Artemia spp.) are used in marine aquaculture worldwide. Annually, more than 2,000 metric tons of dry cysts are used for cultivation of fish, crustacean, and shellfish larva. Brine shrimp are important to aquaculture because newly hatched brine shrimp nauplii (larvae) provide a food source for many fish fry (Mozanzadeh et al., 2021). Culture and harvesting of brine shrimp eggs represents another aspect of the aquaculture industry. Nauplii and metanauplii of Artemia, commonly known as brine shrimp, play a crucial role in aquaculture due to their nutritional value and suitability as live feed for many aquatic species, particularly in larval stages (Sorgeloos & Roubach, 2021).
Or: Beyond linear.
Abstract: Equivariant neural networks are neural networks that incorporate symmetries. The nonlinear activation functions in these networks result in interesting nonlinear equivariant maps between simple representations, and motivate the key player of this talk: piecewise linear representation theory.
Disclaimer: No one is perfect, so please mind that there might be mistakes and typos.
dtubbenhauer@gmail.com
Corrected slides: dtubbenhauer.com/talks.html
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
Unlocking the mysteries of reproduction: Exploring fecundity and gonadosomati...AbdullaAlAsif1
The pygmy halfbeak Dermogenys colletei, is known for its viviparous nature, this presents an intriguing case of relatively low fecundity, raising questions about potential compensatory reproductive strategies employed by this species. Our study delves into the examination of fecundity and the Gonadosomatic Index (GSI) in the Pygmy Halfbeak, D. colletei (Meisner, 2001), an intriguing viviparous fish indigenous to Sarawak, Borneo. We hypothesize that the Pygmy halfbeak, D. colletei, may exhibit unique reproductive adaptations to offset its low fecundity, thus enhancing its survival and fitness. To address this, we conducted a comprehensive study utilizing 28 mature female specimens of D. colletei, carefully measuring fecundity and GSI to shed light on the reproductive adaptations of this species. Our findings reveal that D. colletei indeed exhibits low fecundity, with a mean of 16.76 ± 2.01, and a mean GSI of 12.83 ± 1.27, providing crucial insights into the reproductive mechanisms at play in this species. These results underscore the existence of unique reproductive strategies in D. colletei, enabling its adaptation and persistence in Borneo's diverse aquatic ecosystems, and call for further ecological research to elucidate these mechanisms. This study lends to a better understanding of viviparous fish in Borneo and contributes to the broader field of aquatic ecology, enhancing our knowledge of species adaptations to unique ecological challenges.
Phenomics assisted breeding in crop improvementIshaGoswami9
As the population is increasing and will reach about 9 billion upto 2050. Also due to climate change, it is difficult to meet the food requirement of such a large population. Facing the challenges presented by resource shortages, climate
change, and increasing global population, crop yield and quality need to be improved in a sustainable way over the coming decades. Genetic improvement by breeding is the best way to increase crop productivity. With the rapid progression of functional
genomics, an increasing number of crop genomes have been sequenced and dozens of genes influencing key agronomic traits have been identified. However, current genome sequence information has not been adequately exploited for understanding
the complex characteristics of multiple gene, owing to a lack of crop phenotypic data. Efficient, automatic, and accurate technologies and platforms that can capture phenotypic data that can
be linked to genomics information for crop improvement at all growth stages have become as important as genotyping. Thus,
high-throughput phenotyping has become the major bottleneck restricting crop breeding. Plant phenomics has been defined as the high-throughput, accurate acquisition and analysis of multi-dimensional phenotypes
during crop growing stages at the organism level, including the cell, tissue, organ, individual plant, plot, and field levels. With the rapid development of novel sensors, imaging technology,
and analysis methods, numerous infrastructure platforms have been developed for phenotyping.
The binding of cosmological structures by massless topological defectsSérgio Sacani
Assuming spherical symmetry and weak field, it is shown that if one solves the Poisson equation or the Einstein field
equations sourced by a topological defect, i.e. a singularity of a very specific form, the result is a localized gravitational
field capable of driving flat rotation (i.e. Keplerian circular orbits at a constant speed for all radii) of test masses on a thin
spherical shell without any underlying mass. Moreover, a large-scale structure which exploits this solution by assembling
concentrically a number of such topological defects can establish a flat stellar or galactic rotation curve, and can also deflect
light in the same manner as an equipotential (isothermal) sphere. Thus, the need for dark matter or modified gravity theory is
mitigated, at least in part.
Current Ms word generated power point presentation covers major details about the micronuclei test. It's significance and assays to conduct it. It is used to detect the micronuclei formation inside the cells of nearly every multicellular organism. It's formation takes place during chromosomal sepration at metaphase.
Nucleophilic Addition of carbonyl compounds.pptxSSR02
Nucleophilic addition is the most important reaction of carbonyls. Not just aldehydes and ketones, but also carboxylic acid derivatives in general.
Carbonyls undergo addition reactions with a large range of nucleophiles.
Comparing the relative basicity of the nucleophile and the product is extremely helpful in determining how reversible the addition reaction is. Reactions with Grignards and hydrides are irreversible. Reactions with weak bases like halides and carboxylates generally don’t happen.
Electronic effects (inductive effects, electron donation) have a large impact on reactivity.
Large groups adjacent to the carbonyl will slow the rate of reaction.
Neutral nucleophiles can also add to carbonyls, although their additions are generally slower and more reversible. Acid catalysis is sometimes employed to increase the rate of addition.
Remote Sensing and Computational, Evolutionary, Supercomputing, and Intellige...University of Maribor
Slides from talk:
Aleš Zamuda: Remote Sensing and Computational, Evolutionary, Supercomputing, and Intelligent Systems.
11th International Conference on Electrical, Electronics and Computer Engineering (IcETRAN), Niš, 3-6 June 2024
Inter-Society Networking Panel GRSS/MTT-S/CIS Panel Session: Promoting Connection and Cooperation
https://www.etran.rs/2024/en/home-english/
hematic appreciation test is a psychological assessment tool used to measure an individual's appreciation and understanding of specific themes or topics. This test helps to evaluate an individual's ability to connect different ideas and concepts within a given theme, as well as their overall comprehension and interpretation skills. The results of the test can provide valuable insights into an individual's cognitive abilities, creativity, and critical thinking skills
11. IFN-1
Type 1 Interferons are group of
interferon proteins
Act against viral infection
Functions:
Inhibit hiv replication
Decrease hiv infection in macrophage
RNA degradation
Viral infected cell apoptosis
• INF pDS killer pDS
infected cells killed
13. Role of Dendritic cells
• Dendritic cells- antigen presenting cells
that activates the T-lympocytes
produce INF-1
indoleamin(2,3)dioxygenase
tryptophan catabolism
viral replication inhibited
14. Produce inflammatory cytokine & lyse
the infected cells
Activation receptor:
KIR3DS1,NCRs, NKG 2D
Recognize MHC-1
Kills the infected cells
cDCs IL-12,18 NK cell IFN γ TH1
NK cell DCs CTL response
Role of Natural Killer cells
15. Role of Macrophage
Terminal differentiated, non dividing
cells
Derived from circulating monocyte
Macrophage
MHC-11 MHC-1
T-helper cell Tc cells
activated activated
16. Produce IL-10, IL-27, TGF-beta,
MCSF
Monocyte to Macrophage
differantiation
IL-27
anti HIV
17. Role of Complement system
First-line defender against foreign
pathogens
Classical pathway involved
antibody to envelope
C1q activation
• No Alternative pathway
18. what about lectin pathway??
Lectin pathway occur
Need Mannose Binding Lectin(MBL)
for recognition
But, there is no MBL on HIV.
Then, HOW LECTIN PAHWAY occur?
Answer:
Serum MBL binds on gp120, activates
the lectin pathway
19. Role of Granulocyte
Basophil activated by IgE
releases IL-2 Th2 response occur
Neutrophil express (PD-L1)
Tcell affected negative regulation
Eosinophil
Eosinophilia occur in HIV patients =?
during HIV Th1 response shifted to
Th2 response by IL-4, IL-5. so,
Eosinophil count increases
20. ADAPTIVE IMMUNITY
Host defenses that are mediated by B
cells and T cells following exposure
to antigen and that exhibit specificity,
diversity, memory, and self-non self
discrimination
3 responses involved:
Neutralizing antibody
T-Helper cell response
CTL response
21. Neutralizing Antibodies
Antibodies that bind to pathogen and
prevent it from infecting cells
Block entry of toxin into cell
Target the gp 120 of the HIV
viral transmission stopped
It block transmission of HIV into fetus
Makes HIV as LTNPs- Long Term Non
Progressor
22.
23. Question
HIV changes it’s structure by changing
conformation of gp120, glycosylation
of envelope protein.
If HIV changes it’s structure, how does
the ELISA identification possible???
Answer:
Non Neutralizing antibodies also
produced,. It used in ELISA detection
24. T helper cell response
T helper cells are type T lymphocytes
which recognize MHC11
Produce cytokine that activate
immune cells
Release IL-2, IL-4, IL-5, IL-10, IL-12,
IL-13, TNF –γ
It responsible for the inflammation &
blocking of HIV replication
25. Cytotoxic T lymphocyte
Recognize MHC-1 and lyse the
infected cells
HIV infected cell
MHC-1 Expression
cell lysed
27. Mucosal….
is a lining of mostly endodermal origin. It
consists epithelium , lamina propria
The membranes line present in skin: at
the nostrils, the lips of the mouth,
the eyelids, the ears the genital area,
and the anus.
In the female, the glans clitoridis and
the clitoral hood, and in the male,
the glans penis (the head of the penis)
and the inner layer of the foreskin all
have a mucous membrane.
28. Mucosal Immunity: Innate
level
Epithelial cells & neutrophils produce
antimicrobial peptides
Lysozyme, lactoferin, defensin
disturb
receptors of hiv binding
cells
HIV entry
HIV-1 repelled blocked
29. Mucosal Immunity : Adaptive
level
DCs 1st infected by HIV
bind to DC-SIGN
move to
Lymph node infected cell killed
Vagina & cervix CD4+,CD8+ cells
destroy infected cell
30. Why there is no cure for HIV?
It targets T lymphocytes. So all the
immune activation stopped.
If immune activated, it will kills the T
cells, due to of HIV in it.
Main hero's of immune cells as
MACROPHAGE, WBCs get infected
No immunological Memory formed.
HIV changes it’s structure.