1. Regulatory T cells (Tregs) that express the transcription factor Foxp3 play a key role in controlling immune responses and maintaining immunological self-tolerance. Depletion of Tregs can lead to development of autoimmune diseases and inflammatory conditions.
2. Foxp3 is required for the development and function of Tregs. Mutations that inactivate Foxp3 result in fatal autoimmune diseases in both mice and humans. Depletion of Tregs through the removal of CD25+ cells or neutralization of IL-2 can also induce autoimmunity in normal animals.
3. Tregs constitutively express high levels of CD25 (the IL-2 receptor alpha chain) and depend on IL
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.
Regulatory T cells (Tregs) play an important role in maintaining immune tolerance and suppressing excessive immune responses. Tregs can develop naturally in the thymus or be induced in the periphery. They express the transcription factor FoxP3 and surface markers CD4 and CD25. Tregs suppress the activation and functions of other immune cells and help prevent autoimmunity, control infections, allow transplantation tolerance, and support fetal-maternal tolerance in pregnancy. Dysregulation of Tregs has been linked to immunological diseases. Therapeutic use of Tregs may help treat diseases driven by excessive immune responses like autoimmunity.
Regulatory T-cells (Tregs) help maintain self-tolerance and prevent autoimmunity by suppressing immune responses. They express FOXP3 and CD25 and function through various mechanisms like secreting inhibitory cytokines or metabolizing IL-2. Tregs are implicated in tumor immune escape by suppressing anti-tumor immunity. While Tregs are normally beneficial, in cancer high levels associate with poor prognosis by hindering immune response. Emerging immunotherapies aim to deplete or modulate Tregs to enhance anti-tumor immunity.
Tumor antigens & cancer immunotherapy.pptxRagavi32
Tumor antigens are proteins, glycoproteins, glycolipids, or carbohydrates expressed uniquely on tumor cells. There are two types: tumor specific antigens produced from mutations and tumor associated antigens normally expressed during development but reactivated in cancer. The immune system mounts responses against these antigens via antibodies and cytotoxic T cells to eliminate tumor cells. However, tumors can evolve to escape immune destruction by losing antigen expression or inhibiting immune responses. Immunotherapies aim to enhance antigen presentation, co-stimulation, and pro-inflammatory cytokines to strengthen anti-tumor immunity.
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.
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.
Cytokines are low molecular weight proteins or peptides that are important signaling molecules that regulate immunity and inflammation. They act as intercellular messengers to regulate the intensity and duration of immune responses by binding to receptors on target cells. There are four main structural families of cytokines - hematopoietin receptor family, interferon receptor family, TNF receptor family, and chemokine receptor family. Cytokines can act through autocrine, paracrine, or endocrine signaling and activate signaling pathways like JAK-STAT. An imbalance in the levels of cytokines produced by TH1 and TH2 cells can lead to different disease outcomes. Cytokine-related diseases include septic shock, toxic shock syndrome, and some cancers and infections.
This document summarizes T lymphocyte development and activation. It describes how progenitor cells commit to the T cell lineage in the bone marrow and thymus. In the thymus, T cells undergo proliferation, rearrangement of T cell receptor genes, and positive and negative selection. This results in functionally distinct T cell subsets that migrate to lymph nodes upon activation. T cell activation requires three signals - engagement of the T cell receptor by peptide-MHC complexes, costimulatory molecules such as CD28 binding to B7, and cytokine signals. This leads to intracellular signaling cascades and expression of genes regulating T cell effector function.
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.
Regulatory T cells (Tregs) play an important role in maintaining immune tolerance and suppressing excessive immune responses. Tregs can develop naturally in the thymus or be induced in the periphery. They express the transcription factor FoxP3 and surface markers CD4 and CD25. Tregs suppress the activation and functions of other immune cells and help prevent autoimmunity, control infections, allow transplantation tolerance, and support fetal-maternal tolerance in pregnancy. Dysregulation of Tregs has been linked to immunological diseases. Therapeutic use of Tregs may help treat diseases driven by excessive immune responses like autoimmunity.
Regulatory T-cells (Tregs) help maintain self-tolerance and prevent autoimmunity by suppressing immune responses. They express FOXP3 and CD25 and function through various mechanisms like secreting inhibitory cytokines or metabolizing IL-2. Tregs are implicated in tumor immune escape by suppressing anti-tumor immunity. While Tregs are normally beneficial, in cancer high levels associate with poor prognosis by hindering immune response. Emerging immunotherapies aim to deplete or modulate Tregs to enhance anti-tumor immunity.
Tumor antigens & cancer immunotherapy.pptxRagavi32
Tumor antigens are proteins, glycoproteins, glycolipids, or carbohydrates expressed uniquely on tumor cells. There are two types: tumor specific antigens produced from mutations and tumor associated antigens normally expressed during development but reactivated in cancer. The immune system mounts responses against these antigens via antibodies and cytotoxic T cells to eliminate tumor cells. However, tumors can evolve to escape immune destruction by losing antigen expression or inhibiting immune responses. Immunotherapies aim to enhance antigen presentation, co-stimulation, and pro-inflammatory cytokines to strengthen anti-tumor immunity.
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.
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.
Cytokines are low molecular weight proteins or peptides that are important signaling molecules that regulate immunity and inflammation. They act as intercellular messengers to regulate the intensity and duration of immune responses by binding to receptors on target cells. There are four main structural families of cytokines - hematopoietin receptor family, interferon receptor family, TNF receptor family, and chemokine receptor family. Cytokines can act through autocrine, paracrine, or endocrine signaling and activate signaling pathways like JAK-STAT. An imbalance in the levels of cytokines produced by TH1 and TH2 cells can lead to different disease outcomes. Cytokine-related diseases include septic shock, toxic shock syndrome, and some cancers and infections.
This document summarizes T lymphocyte development and activation. It describes how progenitor cells commit to the T cell lineage in the bone marrow and thymus. In the thymus, T cells undergo proliferation, rearrangement of T cell receptor genes, and positive and negative selection. This results in functionally distinct T cell subsets that migrate to lymph nodes upon activation. T cell activation requires three signals - engagement of the T cell receptor by peptide-MHC complexes, costimulatory molecules such as CD28 binding to B7, and cytokine signals. This leads to intracellular signaling cascades and expression of genes regulating T cell effector function.
T-cells develop in the thymus and include CD4+ T-helper cells, CD8+ cytotoxic T-cells, and regulatory T-cells. T-cells are activated by antigens and signaling molecules and then clonally expand. Activated T-cells have various functions - T-helper cells activate B-cells and mediate cytokine responses; cytotoxic T-cells kill infected or abnormal cells; regulatory T-cells suppress immune responses. T-cells secrete cytokines that regulate immune responses and are involved in B-cell activation, cell-mediated immunity, and autoimmune diseases when dysregulated. T-cells play a crucial role in connecting humoral and cell-mediated immunity.
Cytokines are proteins that are involved in cell signaling and communication during immune responses and inflammation. They modulate processes like immune cell differentiation, activation of lymphocytes and phagocytes, and the development of adaptive immunity. Corticosteroids suppress immunity by blocking cytokine synthesis and release. Cytokines play roles in diseases like cancer, rheumatoid arthritis, and septic shock by regulating immune and inflammatory processes. They can be measured clinically to monitor certain conditions.
The document discusses immuno-oncology and the relationship between cancer and the immune system. It provides an overview of topics that will be covered in an upcoming webinar, including advances in immuno-oncology for different cancer types and combination immunotherapy approaches. The document then reviews key topics in more depth, including how immuno-oncology focuses on improving the body's immune response against cancer and recent immunotherapy approvals. It also discusses how cancer can evade the immune system and strategies for cancer immunotherapy, such as manipulating co-stimulatory signals, enhancing antigen presenting cells, and using cytokines, monoclonal antibodies, and cancer vaccines.
Viruses are obligatory intracellular pathogens that infect cells by utilizing cell surface receptors. The innate immune system responds to viruses through induction of type I interferons like IFN-α and IFN-β, which are produced by infected cells and activate natural killer cells. The adaptive immune system mounts both humoral and cell-mediated responses against viruses. However, viruses have evolved multiple mechanisms to evade the host immune response, such as inhibiting interferon activity, blocking antigen presentation, and inhibiting apoptosis of infected cells.
Cytokine Receptors, Mohammad Mufarreh AliMMufarreh
A detailed description of the nature, types, and mechanisms of action of cytokine receptors.
Describes the different functions of cytokines and their role in the regulation of the immune response.
Cytokine receptor signalling and their regulation and the role of cytokines in disease is also covered briefly.
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.
1. T cells develop from progenitor cells in the thymus and bone marrow through a process involving commitment to the T cell lineage, proliferation, rearrangement of T cell receptor genes, selection processes, and differentiation into mature subsets.
2. Key stages of T cell maturation include double negative, double positive, and single positive stages, driven by signals from the pre-T cell receptor and selection in the thymus.
3. T cell receptor diversity is generated through rearrangement of variable, diversity, and joining gene segments and addition of nucleotides at junctions.
B-cell maturation begins with hematopoietic stem cells in the bone marrow, where they develop through pro-B cell, pre-B cell, and immature B cell stages. During this process, immunoglobulin genes undergo rearrangement and expression of B cell receptors occurs. Immature B cells then migrate to secondary lymphoid tissues to complete maturation. Mature B cells circulate and are activated by antigen to proliferate and differentiate into plasma cells or memory B cells through T cell dependent or independent pathways. T cell dependent activation induces affinity maturation, class switching, and generation of long-lived memory B cells.
Immune tolerance is induced through central and peripheral mechanisms that eliminate or suppress self-reactive immune cells. Central tolerance occurs in the thymus and bone marrow where high-affinity self-reactive T and B cells undergo apoptosis or receptor editing. Peripheral tolerance includes anergy induction, suppression by regulatory T cells (Tregs), and inhibition by receptors like CTLA-4 and PD-1. Tregs expressing the transcription factor FoxP3 are critical for maintaining tolerance and preventing autoimmunity. Failure of these tolerance mechanisms can lead to autoimmune disease.
Cytokines are proteins that mediate communication between cells and help coordinate the body's immune response. They can be divided into groups like lymphokines, monokines, interleukins, and chemokines. Cytokines signal through five main receptor families and activate signaling pathways that induce cellular responses. An imbalance in cytokine signaling has been linked to various diseases. Therapies targeting cytokines and their receptors are used to treat diseases characterized by abnormal cytokine levels like cancer, infections, and autoimmune disorders.
The immune system plays an important role in tumor immunity by recognizing and destroying tumor cells. However, tumors have developed several mechanisms to evade the immune system. Tumors express a variety of tumor antigens that can elicit an immune response, but they often downregulate antigen expression or lose antigenicity over time. Additionally, tumors employ immunosuppressive strategies like increasing immunosuppressive cytokines or reducing co-stimulatory molecules to avoid immune detection and destruction. While immune surveillance exists, tumors have found ways to circumvent it through immune escape mechanisms.
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.
This document discusses cytokines, which are proteins that mediate and regulate the immune system. Some key points:
- Cytokines are produced by multiple cell types and act on multiple cell types in redundant and pleiotropic ways. Their secretion is brief and self-limited.
- They have general functions like mediating innate immunity, regulating lymphocyte growth/activation/differentiation, and activating inflammatory cells or stimulating hematopoiesis.
- Th17 and Treg cells are discussed - Th17 promotes inflammation while Treg prevents effector T cell development and function.
- Cytokine expression and activity are regulated by chromatin structure alterations and the SOCS/CIS family, which inhibit JAK activity or compete
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.
IMMUNE RESPONSE TO TUMORS-Humoral immunity
-Cellular Immunity- Failure of Host Defenses
- Evasion of Immune Responses by Tumors
- Cancer Immunosurveillance vs Immunoediting- Immunotherapy
B cell Activation by T Independent & T Dependent Antigens-Dr C R MeeraMeera C R
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.
Central tolerance refers to deletion of self-reactive T and B cells in the thymus and bone marrow during maturation. T cells that recognize self antigens undergo apoptosis in the thymus. Peripheral tolerance uses backup mechanisms like clonal deletion through activation-induced cell death, clonal anergy from lack of co-stimulation, and suppression by regulatory T cells. These mechanisms help prevent autoimmune disease by silencing self-reactive cells that escape central tolerance.
Regulatory T cells (Tregs), formerly known as suppressor T cells, are a subset of T cells that modulate the immune system and maintain tolerance to self-antigens. They suppress immune responses and help prevent autoimmune disease and cancer. Tregs develop in the thymus from progenitor cells, where they express the transcription factor Foxp3 and are selected to recognize self-MHC molecules. They have a diverse T cell receptor repertoire biased toward self-peptides.
This document discusses research on using regulatory T cells (Tregs) for graft-versus-host disease (GVHD) prevention after allogeneic hematopoietic cell transplantation (HCT). Key points include:
1) Tregs show promise in controlling GVHD while retaining the graft-versus-leukemia effect in mouse models of allogeneic HCT.
2) Studies demonstrate that higher levels of Tregs early after HCT in patients correlate with less severe acute GVHD.
3) Researchers have developed methods to successfully expand Tregs from umbilical cord blood (CB) through CD25 selection and CD3/CD28 bead stimulation while maintaining a functional
T-cells develop in the thymus and include CD4+ T-helper cells, CD8+ cytotoxic T-cells, and regulatory T-cells. T-cells are activated by antigens and signaling molecules and then clonally expand. Activated T-cells have various functions - T-helper cells activate B-cells and mediate cytokine responses; cytotoxic T-cells kill infected or abnormal cells; regulatory T-cells suppress immune responses. T-cells secrete cytokines that regulate immune responses and are involved in B-cell activation, cell-mediated immunity, and autoimmune diseases when dysregulated. T-cells play a crucial role in connecting humoral and cell-mediated immunity.
Cytokines are proteins that are involved in cell signaling and communication during immune responses and inflammation. They modulate processes like immune cell differentiation, activation of lymphocytes and phagocytes, and the development of adaptive immunity. Corticosteroids suppress immunity by blocking cytokine synthesis and release. Cytokines play roles in diseases like cancer, rheumatoid arthritis, and septic shock by regulating immune and inflammatory processes. They can be measured clinically to monitor certain conditions.
The document discusses immuno-oncology and the relationship between cancer and the immune system. It provides an overview of topics that will be covered in an upcoming webinar, including advances in immuno-oncology for different cancer types and combination immunotherapy approaches. The document then reviews key topics in more depth, including how immuno-oncology focuses on improving the body's immune response against cancer and recent immunotherapy approvals. It also discusses how cancer can evade the immune system and strategies for cancer immunotherapy, such as manipulating co-stimulatory signals, enhancing antigen presenting cells, and using cytokines, monoclonal antibodies, and cancer vaccines.
Viruses are obligatory intracellular pathogens that infect cells by utilizing cell surface receptors. The innate immune system responds to viruses through induction of type I interferons like IFN-α and IFN-β, which are produced by infected cells and activate natural killer cells. The adaptive immune system mounts both humoral and cell-mediated responses against viruses. However, viruses have evolved multiple mechanisms to evade the host immune response, such as inhibiting interferon activity, blocking antigen presentation, and inhibiting apoptosis of infected cells.
Cytokine Receptors, Mohammad Mufarreh AliMMufarreh
A detailed description of the nature, types, and mechanisms of action of cytokine receptors.
Describes the different functions of cytokines and their role in the regulation of the immune response.
Cytokine receptor signalling and their regulation and the role of cytokines in disease is also covered briefly.
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.
1. T cells develop from progenitor cells in the thymus and bone marrow through a process involving commitment to the T cell lineage, proliferation, rearrangement of T cell receptor genes, selection processes, and differentiation into mature subsets.
2. Key stages of T cell maturation include double negative, double positive, and single positive stages, driven by signals from the pre-T cell receptor and selection in the thymus.
3. T cell receptor diversity is generated through rearrangement of variable, diversity, and joining gene segments and addition of nucleotides at junctions.
B-cell maturation begins with hematopoietic stem cells in the bone marrow, where they develop through pro-B cell, pre-B cell, and immature B cell stages. During this process, immunoglobulin genes undergo rearrangement and expression of B cell receptors occurs. Immature B cells then migrate to secondary lymphoid tissues to complete maturation. Mature B cells circulate and are activated by antigen to proliferate and differentiate into plasma cells or memory B cells through T cell dependent or independent pathways. T cell dependent activation induces affinity maturation, class switching, and generation of long-lived memory B cells.
Immune tolerance is induced through central and peripheral mechanisms that eliminate or suppress self-reactive immune cells. Central tolerance occurs in the thymus and bone marrow where high-affinity self-reactive T and B cells undergo apoptosis or receptor editing. Peripheral tolerance includes anergy induction, suppression by regulatory T cells (Tregs), and inhibition by receptors like CTLA-4 and PD-1. Tregs expressing the transcription factor FoxP3 are critical for maintaining tolerance and preventing autoimmunity. Failure of these tolerance mechanisms can lead to autoimmune disease.
Cytokines are proteins that mediate communication between cells and help coordinate the body's immune response. They can be divided into groups like lymphokines, monokines, interleukins, and chemokines. Cytokines signal through five main receptor families and activate signaling pathways that induce cellular responses. An imbalance in cytokine signaling has been linked to various diseases. Therapies targeting cytokines and their receptors are used to treat diseases characterized by abnormal cytokine levels like cancer, infections, and autoimmune disorders.
The immune system plays an important role in tumor immunity by recognizing and destroying tumor cells. However, tumors have developed several mechanisms to evade the immune system. Tumors express a variety of tumor antigens that can elicit an immune response, but they often downregulate antigen expression or lose antigenicity over time. Additionally, tumors employ immunosuppressive strategies like increasing immunosuppressive cytokines or reducing co-stimulatory molecules to avoid immune detection and destruction. While immune surveillance exists, tumors have found ways to circumvent it through immune escape mechanisms.
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.
This document discusses cytokines, which are proteins that mediate and regulate the immune system. Some key points:
- Cytokines are produced by multiple cell types and act on multiple cell types in redundant and pleiotropic ways. Their secretion is brief and self-limited.
- They have general functions like mediating innate immunity, regulating lymphocyte growth/activation/differentiation, and activating inflammatory cells or stimulating hematopoiesis.
- Th17 and Treg cells are discussed - Th17 promotes inflammation while Treg prevents effector T cell development and function.
- Cytokine expression and activity are regulated by chromatin structure alterations and the SOCS/CIS family, which inhibit JAK activity or compete
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.
IMMUNE RESPONSE TO TUMORS-Humoral immunity
-Cellular Immunity- Failure of Host Defenses
- Evasion of Immune Responses by Tumors
- Cancer Immunosurveillance vs Immunoediting- Immunotherapy
B cell Activation by T Independent & T Dependent Antigens-Dr C R MeeraMeera C R
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.
Central tolerance refers to deletion of self-reactive T and B cells in the thymus and bone marrow during maturation. T cells that recognize self antigens undergo apoptosis in the thymus. Peripheral tolerance uses backup mechanisms like clonal deletion through activation-induced cell death, clonal anergy from lack of co-stimulation, and suppression by regulatory T cells. These mechanisms help prevent autoimmune disease by silencing self-reactive cells that escape central tolerance.
Regulatory T cells (Tregs), formerly known as suppressor T cells, are a subset of T cells that modulate the immune system and maintain tolerance to self-antigens. They suppress immune responses and help prevent autoimmune disease and cancer. Tregs develop in the thymus from progenitor cells, where they express the transcription factor Foxp3 and are selected to recognize self-MHC molecules. They have a diverse T cell receptor repertoire biased toward self-peptides.
This document discusses research on using regulatory T cells (Tregs) for graft-versus-host disease (GVHD) prevention after allogeneic hematopoietic cell transplantation (HCT). Key points include:
1) Tregs show promise in controlling GVHD while retaining the graft-versus-leukemia effect in mouse models of allogeneic HCT.
2) Studies demonstrate that higher levels of Tregs early after HCT in patients correlate with less severe acute GVHD.
3) Researchers have developed methods to successfully expand Tregs from umbilical cord blood (CB) through CD25 selection and CD3/CD28 bead stimulation while maintaining a functional
This document discusses potential cell surface markers that could reliably identify CD4+CD25+ regulatory T cells. It notes that while CD25, GITR, and CTLA-4 have been used as markers, they are not specific to regulatory T cells alone. The document suggests several potential new markers for regulatory T cells, such as galectin-1, CD103, Ly6, 4-1BB, and neuropilin-1, but notes there may be still unidentified markers labeled X, Y, Z. It concludes there is a need to find better markers that uniquely identify regulatory T cells.
Regulatory T cells (Tregs) play a critical role in maintaining immune homeostasis. There are two main types of Tregs: natural Tregs that develop in the thymus and express CD4 and CD25, and adaptive Tregs that acquire expression of CD25 in tissues outside the thymus during inflammation. Tregs exert their immunosuppressive effects through several mechanisms, including secreting cytokines like IL-10 and TGF-beta, expressing molecules like CTLA-4 that inhibit other immune cells, and inducing apoptosis in effector T cells. Adaptive Tregs mature in peripheral tissues under the influence of TGF-beta, where they gain expression of Treg markers and Foxp3, allowing them to se
Regulatory T cells, also known as T-regs, are a recently discovered subset of immune cells that play a key role in suppressing autoimmune responses and maintaining self-tolerance. T-regs express the cell surface marker CD25 and the transcription factor Foxp3, which gives them their suppressive properties. Ongoing research is helping to elucidate the mechanisms by which T-regs regulate other immune cells and prevent autoimmunity. Manipulation of T-regs may offer new therapies for autoimmune diseases and conditions involving transplant rejection or unwanted immune responses.
This document summarizes research on regulatory T cells (Tregs) and their implications in graft-versus-host disease (GVHD). It discusses:
1) Tregs play an important role in maintaining immune homeostasis and preventing autoimmune diseases like GVHD.
2) Preclinical studies show that Treg depletion leads to worse GVHD in mice, while Treg adoptive transfer mitigates GVHD.
3) Clinical trials testing Treg immunotherapy for GVHD prevention and treatment have shown promising results, but more research is still needed to fully understand Treg subsets and develop effective Treg-based therapies.
T helper 17 cells (Th17) are a subset of T helper cells producing interleukin 17 (IL-17). They are developmentally distinct from Th1 and Th2 cells.
They create inflammation and tissue injury in autoimmune disease
T cells can be categorized into several subsets including helper T cells, cytotoxic T cells, memory T cells, and regulatory T cells. Helper T cells assist other immune cells, cytotoxic T cells destroy infected and tumor cells, memory T cells provide faster responses upon reexposure to pathogens, and regulatory T cells suppress immune activation and prevent autoimmunity. Understanding regulatory T cells in HIV-1 could lead to new immunotherapy or vaccine strategies, but their exact role in HIV-1 pathogenesis requires further study.
The IEM Cancer Animal Core Lab provides housing, handling, and experimental support services for small animal cancer research. It maintains several mouse and rat cancer models, including prostate, breast, and pancreatic cancers. Services include animal care, cell culture, tumor implantation and monitoring, imaging such as dorsal skinfold chamber and photoacoustic imaging, and histology. Pricing ranges from $500 for basic studies to $2,200 for more complex models like dorsal skinfold chamber. The core aims to reduce the time and effort for investigators to conduct pilot and long-term cancer studies using pre-existing models.
This document contains information about a student named Archana V.T. who is studying mathematics at K.T.C.T. College of Teacher Education in Kaduvayil. It includes her name, subject of study, and registration number.
T-lymphocytes can only be activated by antigen complexes with HLA antigens from the person the lymphocytes originated from. During development in the thymus, lymphocytes that react with self-antigens presented by HLA die while those that recognize foreign antigens with a low affinity survive in a process called positive selection. Negatively selecting eliminates lymphocytes that react strongly to self-antigens. This results in a T-cell population that can recognize foreign peptides bound to self-HLA molecules.
Este documento presenta los objetivos de una clase sobre las células T efectores Th17. Los objetivos incluyen comprender los estímulos que conducen a la diferenciación de células Th17 y sus mecanismos de acción, así como identificar los puntos de control moleculares involucrados en el desarrollo, activación, diferenciación y regulación de la respuesta de las células Th17. También se describen brevemente las funciones efectrices de las células T CD4 y CD8, y los mecanismos de diferenciación de las cél
This document discusses T helper 17 cells and their role in autoimmune diseases. It contains 3 figures: Figure 1 shows T cells and macrophages entering the central nervous system in a mouse model of multiple sclerosis, Figure 2 outlines the cytokines required for generating TH17 cells, and Figure 3 depicts the reciprocal expression of Foxp3 and IL-17 during T cell differentiation. The document also briefly mentions several autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and Crohn's disease, and potential molecular targeted therapies for these conditions including antibodies against TNF-α, IL-6, and possibly IL-17 in the future.
1) The document discusses iron status tests including serum iron, total iron binding capacity, and ferritin.
2) It describes the principles, reagents, and normal ranges for serum iron and total iron binding capacity tests performed using a manual method.
3) Details are provided on the preparation of deionized water, hydrochloric acid, iron standards, and chromogens used in the tests.
This document discusses maternal immunity transfer in teleost fish. It describes how various immune factors like immunoglobulins, complement components, lysozymes, lectins, and yolk proteins are transferred from mother to offspring to provide protection. This transfer is critical because fish eggs have closed systems and offspring rely on maternal immunity before developing their own immune systems. The document outlines the modes of transfer and factors that can influence it, as well as potential applications for improving fish culture through maternal immunity priming.
This document discusses transplantation immunology and organ transplantation. It begins by defining transplantation as taking cells, tissues, or organs from one individual and placing them into another. It describes different types of grafts, including autologous, syngeneic, allogeneic, and xenogeneic grafts. It then discusses transplantation antigens such as major histocompatibility antigens and minor histocompatibility antigens. It explains the mechanisms of graft rejection, including T-cell mediated rejection, antibody-mediated rejection, and NK cell mediated rejection. It also covers preventing rejection through matching transplantation antigens and using immunosuppressive drugs like calcineurin inhibitors and IMPDH inhibitors.
The document discusses T cell development and selection in the thymus. Immature T cells enter the thymus with a random T cell receptor (TCR) repertoire that includes receptors harmful to the body. The thymus subjects these cells to positive and negative selection to purge harmful self-reactive cells and retain those useful for foreign antigen recognition in a process that establishes T cell tolerance. Positively selected cells have TCRs that recognize self-MHC molecules, making their recognition MHC-restricted and useful for the immune response.
The immune system consists of cells and molecules that respond to foreign substances. Innate immunity provides early defenses through physical barriers, phagocytic cells, complement proteins, and cytokines. Adaptive immunity develops specific responses through cellular immunity mediated by T cells and humoral immunity mediated by antibodies from B cells. Together, the innate and adaptive immune responses provide protection from pathogens while avoiding reactivity to self.
Upon encountering antigen, naive T cells are activated and differentiate into effector T cells. Dendritic cells carry antigens from infection sites to secondary lymphoid tissues where they present antigen to naive T cells. Naive T cells recirculate through secondary lymphoid tissues via blood and lymph and encounter antigen on antigen presenting cells, leading to their activation and differentiation. Cell adhesion molecules and chemokines mediate the trafficking of naive T cells to secondary lymphoid tissues where they can encounter antigen.
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:
1) Munn's 1999 discovery that IDO suppresses T-cell mediated rejection of tumors and fetal allografts by depleting tryptophan.
2) Mechanistic studies showing IDO induces T-cell arrest and inhibits proliferation through tryptophan depletion and kynurenine production, leading to Treg differentiation and CTL inhibition.
3) Preclinical studies combining IDO inhibitors with chemotherapy or vaccines, showing enhanced anti-tumor effects.
4) Ongoing clinical
The document discusses how infection can be detrimental for patients with mitochondrial disease due to the increased energy demands and potential immune dysfunction. It outlines how the immune system may be compromised in mitochondrial disease based on clinical observations of increased infections and poor vaccine responses in some patients. Animal studies show that mitochondrial dysfunction within immune cells can impair their function and response to infection.
1) The document discusses tumor immunology and mechanisms of tumor immune evasion. It describes how tumors can downregulate MHC expression, secrete immunosuppressive factors, inhibit T cell function through checkpoint pathways like PD-1/PD-L1, and recruit immunosuppressive cells like Tregs.
2) Checkpoint pathways like CTLA-4 and PD-1 normally regulate T cell activation, but tumors can exploit these pathways to evade immune destruction by overexpressing ligands that bind these inhibitory receptors.
3) Several immunotherapies targeting CTLA-4 and PD-1/PD-L1 have been developed including ipilimumab, nivolumab, pembrol
Three sentences summarizing the key points:
1) Infection can be detrimental for patients with mitochondrial disease as it increases their metabolic demands and immune responses can further damage mitochondria.
2) Some patients with mitochondrial disease may have immune dysfunction, shown by recurrent infections, hypogammaglobulinemia, poor vaccine responses, and impaired clearance of viruses.
3) The NIH MINI study aims to characterize immune function and risks of infection in mitochondrial disease patients through longitudinal monitoring to help mitigate health risks.
1) Bacteria that normally live in the gut can have either symbiotic or pathogenic relationships with their human host. Pathogenic bacteria produce virulence factors that subvert the host's immune defenses, while symbiotic bacteria may secrete regulatory molecules that modulate immunity.
2) The human microbiota interacts with multiple organ systems beyond the gut, influencing metabolism, inflammation, and other physiological processes through molecular signals. Understanding these host-microbiota interactions could lead to new treatments.
3) Studies on the bacterial effector proteins secreted by pathogens like Shigella provide insights into how innate and adaptive immune responses are activated or suppressed. This knowledge may help design new antimicrobials and vaccines.
Immunology of tanslanatation and malignancyraghunathp
This document discusses immunology of transplantation and malignancy. It defines transplantation as transferring cells, tissues or organs from one site to another. The first- and second-set rejection of allografts is described, where a second graft from the same donor is rejected more quickly. Tumor cells can induce immune responses as they express new antigens foreign to the host. However, tumors can escape immunosurveillance through various mechanisms like weak immunogenicity or suppression of the immune response. Immunotherapy approaches aim to enhance these immune responses through both active and passive methods.
- Cancer remains a leading cause of death globally, with an estimated 12.7 million cases expected to increase to 21 million by 2030.
- Tumors can be detected through abnormal cell proliferation caused by genetic mutations or loss of growth control.
- The immune system responds to tumor antigens expressed by cancer cells and tumor-associated antigens shared between tumors induced by the same virus.
- However, tumors have developed multiple mechanisms to evade immune surveillance such as low immunogenicity, antigen modulation, immune suppression, and inducing lymphocyte apoptosis.
1. The document discusses mechanisms of immunological tolerance and the pathogenesis of autoimmune diseases. It describes how central and peripheral tolerance lead to the deletion or inactivation of self-reactive lymphocytes.
2. A loss of tolerance can occur through molecular mimicry with infectious agents, exposure of sequestered antigens, hormonal influences, and genetic factors. This can lead to tissue damage through various effector mechanisms like antibody-mediated cytotoxicity.
3. Examples are given of organ-specific autoimmune diseases associated with certain autoantibodies, as well as immune complex-mediated conditions like vasculitis. Therapeutic approaches aim to restore tolerance or suppress effector responses.
- Cancer remains a leading cause of death globally, with an estimated 12.7 million cases in the world currently that is expected to rise to 21 million by 2030.
- Tumors develop due to the abnormal and uncontrolled proliferation of cells caused by genetic mutations or damage from carcinogens like radiation, chemicals, or viruses.
- The immune system can recognize and attack tumor cells through mechanisms like antigen presentation, cytotoxic T-cells, antibodies, and natural killer cells. However, tumors also have ways to evade the immune system such as low immunogenicity or immunosuppressive tactics.
- Modern cancer immunotherapy harnesses the immune system through approaches like monoclonal antibodies, cytokines, adoptive cell therapy, and
TRANSPLANTATION AND TUMOUR IMMUNITY (1).pptxfaria824398
Transfer of cells, tissues or organs from one individual to another or from one site in the same individual is known as Transplantation.
Graft rejection is due to the reaction of the host to the grafted tissue (host-versus-graft response).
This document discusses the immune response to helminth infections in three parts. It begins by describing the innate and adaptive immune responses that lead to rejection of helminths, including the roles of cytokines, antibodies, granulocytes, and T cells. It then explains how helminths evade and modulate the immune system to establish chronic infections, such as through regulatory T cells, alternatively activated macrophages, and cytokines like IL-10 and TGF-β that suppress inflammation. Finally, it concludes that while immunomodulation benefits the host by reducing immune-mediated damage, it can also increase susceptibility to other pathogens.
Biology 106 Journal 3 ( Mader 13) Lvmphatic System and.docxhartrobert670
Biology 106
Journal 3 ( Mader 13)
Lvmphatic System and Immunity Chapter
Read Chapter 7 and Infectious Diseases Supplement (enclosed) or use ebook in Connect Plus
DO: chapter questions page 151
Questions 1-10-16
17. What is Lupus? How did Abigail get the disease? Should she worry? Why is it called an
autoimmune disease?
18. What are some common autoimmune diseases? What reaction in the body causes
autoimmune diseases? Can they be treated?
Be able to answer the multiple choice questions 16-36. Check your answers!!
Read: The Vaccine Controversy. Truth or Consequences
And answer the following questions:
1. What is a vaccine?
2. What is Hib meningitis? When did a vaccine to prevent this disease become available?
3. In 1796, Edward Jenner developed a vaccine against what disease? How?
4. In 1998, a backlash against childhood immunizations began, why? Did scientists find
any validity against the claims? How were they disproven?
5. What are some myths and misconceptions about vaccines and what is the truth?
6. What is herd immunity? Why is it important to vaccinate as many members of a
community as possible?
7. How many cases of measles occurred in France 2-3 years ago? This year? Why?
8. What is pertussis, and what are its symptoms? Why are we getting new outbreaks in a
disease that was once under control?
9. What are some vaccinations that you had?
10. Should unvaccinated children be permitted in public schools?
~IDS Discussion
A. Handouts
B. Infectious disease Supplement
C. web sites These may help you - you may use any reputable website.
http://www. aidsinfo. nih. gov/
www.amfar.org/
Read and bring in any new information that you find and wish to share. Information on
AIDS is constantly being updated.
1. What is a virus? What is a host
2. What does the acronym AIDS represent. How about HIV virus?
3. What are retroviruses? What are some other retroviruses?
4. How is AIDS transmitted? What 3 enzymes do they contain that allow replication to occur
5. What is an opportunistic infection? What opportunistic infections or diseases might a person
with AIDS get?
6. Why is AIDS considered such a global health issue?
7. What are the special problems of AIDS in poor and developing countries?
8. What treatments are currently available. What is the problem with the available treatments
(side effects)?
9. What is the status of an AIDS vaccine?
10. Do we still need to worry about AIDS and can we stop being cautious?
Using the Supplement
Answer
1. What are the effects of tuberculosis? Do we need to worry about it anymore?
2. What is the cause of malaria? What is the best way to prevent it? Can people in the US
get malaria?
3. Where do emerging diseases come from?
4. What causes SARS?
5. What causes MRSA? What are the symptoms ofMRSA? How can we reduce the
incidence ofMRSA?
• Activated T cells undergo clonal expansion until the illness has
been stemmed. Then, most of the activated T ...
The document provides an overview of immunology topics covered in a course, including the immune system and disease, immunopathology, and therapeutic applications. The course covers basics of the immune system, innate and adaptive immunity, cells and molecules of the immune system, and applications like immunization, transplantation, and immunotherapy. Immunopathology topics include immunodeficiency, autoimmunity, hypersensitivity, and malignancies of the immune system. Therapeutic applications focus on immunization, immunomodulation, transplantation, immunosuppression, and replacement therapies.
This document summarizes a lecture on immunology. It discusses the components of the immune system including leukocytes, lymphoid tissues, and recognition of self. It describes innate immunity mechanisms like physical barriers and phagocytosis. Adaptive immunity involves humoral responses from B cells and cell-mediated responses from T cells. Immune disorders result from failures to distinguish self from non-self, like in autoimmune diseases, or from immunodeficiency, as in AIDS. The learning outcomes cover the immune system's structures, innate and adaptive immunity differences, innate immunity processes, adaptive immunity features, and immune disorder pathophysiology.
Adaptive immunity 2 - Immune regulatory mechanisms through B cell axisVICTOR MAESTRE RAMIREZ
1) The document discusses regulatory B cells that suppress autoimmune diseases by producing the anti-inflammatory cytokine IL-10.
2) Studies in mice show that plasmablasts, a type of short-lived B cell, are the main producers of IL-10 in lymph nodes during experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis.
3) These plasmablasts suppress EAE by migrating to the T cell-B cell border in lymph nodes, where they inhibit dendritic cells and prevent the differentiation of autoreactive T cells through IL-10 signaling.
This document provides an overview of transplantation immunology. It discusses the types of transplants including autografts, isografts, allografts, and xenografts. It describes how the immune system recognizes and rejects foreign grafts through cell-mediated and antibody-mediated responses. Major histocompatibility complexes play an important role in graft rejection. Immunosuppressive drugs can help prevent rejection but come with side effects. While organ transplantation saves lives, the shortage of donor organs remains a challenge.
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.
Dr. Santos Manes - Simposio Internacional 'Terapias oncológicas avanzadas'Fundación Ramón Areces
Los días 15 y 16 de octubre de 2014, la Fundación Ramón Areces y la Real Academia Nacional de Farmacia, en colaboración con la Fundación de la Innovación Bankinter, reunieron en Madrid a algunos de los mayores expertos mundiales en nuevas terapias contra el cáncer. El Simposio Internacional, coordinado por la profesora y académica María José Alonso, analizó el momento actual de la lucha contra esta enfermedad. También fue un punto de encuentro para científicos de los más innovadores institutos de investigación en oncología, quienes debatieron sobre tres grandes temas: la Medicina Personalizada contra el cáncer, los nanomedicamentos en la terapia del cáncer y las terapias basadas en la inmunomodulación.
Similar to Control of immune response by regulatory T cells (20)
Victor Maestre Ramirez has been awarded a certificate numbered 33,423,704 for successfully completing the 4 hour online course "Intermediate Deep Learning with PyTorch" on April 13, 2024.
Gestión de Incidentes de Cibersegurdad - Centro Criptológico NacionalVICTOR MAESTRE RAMIREZ
El documento certifica que Víctor Maestre Ramírez ha completado con éxito un curso de 15 horas sobre Gestión de Incidentes de Ciberseguridad del 7 de abril de 2024. El curso cubrió temas como introducción a incidentes de ciberseguridad, su clasificación, gestión e incidentes, notificación de incidentes y herramientas recomendadas.
Víctor Maestre Ramírez completed a course on modern performance management on March 23, 2024 at 7:13PM UTC, which lasted 57 minutes. The course covered performance management skills and was provided by an education provider approved by the Project Management Institute. Victor received 0.75 PDUs or contact hours for completing the course and was provided a certificate of completion.
Victor Maestre Ramirez has been awarded a certificate numbered 33,235,113 for successfully completing a 4-hour course titled "Deep Learning for Images with PyTorch" on March 21, 2024.
Víctor Maestre Ramírez completed a course on values-based management on March 03, 2024, spending 1 hour and 3 minutes. The course covered management skills and provided 1 PDU. The certificate ID for the course is listed.
Víctor Maestre Ramírez completed a course on Artificial Intelligence for Business Leaders that covered skills in Artificial Intelligence for Business and Artificial Intelligence. The course took 1 hour and 33 minutes to complete on February 25, 2024 at 8:16PM UTC. A certificate was issued with a unique identification number.
Congestive Heart failure is caused by low cardiac output and high sympathetic discharge. Diuretics reduce preload, ACE inhibitors lower afterload, beta blockers reduce sympathetic activity, and digitalis has inotropic effects. Newer medications target vasodilation and myosin activation to improve heart efficiency while lowering energy requirements. Combination therapy, following an assessment of cardiac function and volume status, is the most effective strategy to heart failure care.
Applications of NMR in Protein Structure Prediction.pptxAnagha R Anil
This presentation explores the pivotal role of Nuclear Magnetic Resonance (NMR) spectroscopy in predicting protein structures. It delves into the methodologies, advancements, and applications of NMR in determining the three-dimensional configurations of proteins, which is crucial for understanding their function and interactions.
Fexofenadine is sold under the brand name Allegra.
It is a selective peripheral H1 blocker. It is classified as a second-generation antihistamine because it is less able to pass the blood–brain barrier and causes lesser sedation, as compared to first-generation antihistamines.
It is on the World Health Organization's List of Essential Medicines. Fexofenadine has been manufactured in generic form since 2011.
Discover the benefits of homeopathic medicine for irregular periods with our guide on 5 common remedies. Learn how these natural treatments can help regulate menstrual cycles and improve overall menstrual health.
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The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
congenital GI disorders are very dangerous to child. it is also a leading cause for death of the child.
this congenital GI disorders includes cleft lip, cleft palate, hirchsprung's disease etc.