Immunity
Immunity
Innate: Immediate, Natural, always present(innate), Block and rapidly eliminate microbes.
Adaptive: Slow and specialized, acquired/specific, expansion and differentiation of lymphocytes in response to microbes before it can provide an effective defense.
Lymphocytes: specific recognition of Antigens.
B Lymphocytes: Mediators of Humoral immunity.
T Lymphocytes: Mediators in cell-mediated immunity.
Antigen Presenting Cells: Capture of antigens for a display to Lymphocytes.
Dendritic cells: initiation of T cell responses.
Macrophages: effector phase of cell-mediated immunity
Follicular dendritic cells: the display of antigens to B lymphocytes in humoral immune responses.
Effector Cells: T lymphocytes, Macrophages, Granulocytes.
T Lymphocytes: activation of phagocytes, killing infected cells.
Macrophages: Phagocytosis and killing of microbes.
Granulocytes: Killing microbes.
Generative lymphoid organs: bone marrow (B lymphocytes and myeloid cells), Thymus (T lymphocytes).
Peripheral Lymphoid organs: Lymph system, skin, lymph nodes and vessels, spleen.
Pathogen associated Molecular Patterns: innate cells express receptors that recognize molecular structures produced by microbial pathogens.
Damage Associated Molecular Patterns: Innate receptors can be activated by damage to cells.
Pattern recognition Receptors: Receptors that recognize PAMPS and DAMPS)
Innate immune cells recognise a PAMP or DAMPà Capture, engulfment and destruction or Display of antigen to other cells.
Innate cells: Macrophages and dendritic cells that can phagocytose microbes.
Phagocytosis: recognition and attachment of PRR on the cell surface, Engulfment, Killing, and degradation.
Phagocytosis degradation: Reactive O species, nitric oxide, lysosomal enzymes.
Adaptive immune system capable of recognising 10^7-10^9.
PRR recognition: Humoral immune response or cell-mediated immune response.
Humoral immunity: mediated by antibodies produced by B cells, antibodies recognise microbial antigens neutralise their infectivity and target microbes for elimination (mainly extracellular).
Cell mediated immunity: Mediated by T cells and their produced cytokines (Mainly intracellular).
Immunologic Memory: subsequent exposures to the same antigen are faster, larger, as each exposure to an antigen generates long-lived antigen-specific memory cells, return the immune system to homeostasis faster.
Innate immune system: Fast as microbes can multiply fast, release phagocytes, inflammatory cytokines and interferons/antivirals, Cytokines.
Adaptive Immune system: takes 6-7 days.
Innate immune system recognises PAMPS and DAMPS with PPR’s
Epithelial Barrier: Physical barrier, Produce antimicrobial chemicals (direct toxicity or activation of other Leukocytes), Intraepithelial T cells recognise small number of common microbial structures (Cytokine Production and Phagocyte activation)
Phagocytes: Neutrophils and monocytes, Macrophages (recruited from blood into infected tissues in response to signals from sentinel cells).
Dendritic cells: Express many PRR, versatile sensor of PAMPS and DAMPS, capable of triggering and directing adaptive T cell mediated immune response(present In epithelia and most tissues)( uptake & transport of antigens to lymph nodes, upregulation of costimulators, production of cytokines).
Natural Killer cells: Kill infected cells via granule exocytosis of perforin and granzyme proteins adjacent to target cells, Produce Cytokine interferon (IFN)-y to increase the capacity of macrophages to kill phagocytosed bacteria.
Soluble components: recognize microbes and/or promote innate/adaptive responses
Complements: Culminate in the production of peptides that stimulate inflammation (C3a, C5a) and polymerized C6-C9 which form membrane attack complex.
cytokines: Signalling molecules that aid cell to cell communication in immune response and stimulate movement of cells toward sites of inflammation, infection and trauma.
Inflammation: Bring leukocytes and plasma proteins to the site of infection or tissue damage, eliminate the cause and initiate healing.
Inflammation symptoms: Redness, Heat , Swelling (Leakage of cells and fluid into tissues), Pain (Increased nerve sensitivity due to chemical mediators).
Inflammatory process: Offending agent recognized by host cell/molecules > produce chemical mediators, Leukocytes and plasma proteins recruited from circulation > activated to destroy and eliminate offending substance, Reaction is controlled and terminated damaged tissue repaired.
resolution of inflammation: normal permeability, Drainage of fluid & proteins into lymph, Pinocytosis into macrophages, Phagocytosis of apoptotic neutrophils, Phagocytosis of necrotic debris, Disposal of macrophages.
Type 1 Interferons: Bind onto uninfected cells inducing the expression of enzymes that block viral replication > turns on an antiviral state.
Infected cell: produce type 1 interferons that bind onto uninfected cells.
Immunity
Innate: Immediate, Natural, always present(innate), Block and rapidly eliminate microbes.
Adaptive: Slow and specialized, acquired/specific, expansion and differentiation of lymphocytes in response to microbes before it can provide an effective defense.
Lymphocytes: specific recognition of Antigens.
B Lymphocytes: Mediators of Humoral immunity.
T Lymphocytes: Mediators in cell-mediated immunity.
Antigen Presenting Cells: Capture of antigens for a display to Lymphocytes.
Dendritic cells: initiation of T cell responses.
Macrophages: effector phase of cell-mediated immunity
Follicular dendritic cells: the display of antigens to B lymphocytes in humoral immune responses.
Effector Cells: T lymphocytes, Macrophages, Granulocytes.
T Lymphocytes: activation of phagocytes, killing infected cells.
Macrophages: Phagocytosis and killing of microbes.
Granulocytes: Killing microbes.
Generative lymphoid organs: bone marrow (B lymphocytes and myeloid cells), Thymus (T lymphocytes).
Peripheral Lymphoid organs: Lymph system, skin, lymph nodes and vessels, spleen.
Pathogen associated Molecular Patterns: innate cells express receptors that recognize molecular structures produced by microbial pathogens.
Damage Associated Molecular Patterns: Innate receptors can be activated by damage to cells.
Pattern recognition Receptors: Receptors that recognize PAMPS and DAMPS)
Innate immune cells recognise a PAMP or DAMPà Capture, engulfment and destruction or Display of antigen to other cells.
Innate cells: Macrophages and dendritic cells that can phagocytose microbes.
Phagocytosis: recognition and attachment of PRR on the cell surface, Engulfment, Killing, and degradation.
Phagocytosis degradation: Reactive O species, nitric oxide, lysosomal enzymes.
Adaptive immune system capable of recognising 10^7-10^9.
PRR recognition: Humoral immune response or cell-mediated immune response.
Humoral immunity: mediated by antibodies produced by B cells, antibodies recognise microbial antigens neutralise their infectivity and target microbes for elimination (mainly extracellular).
Cell mediated immunity: Mediated by T cells and their produced cytokines (Mainly intracellular).
Immunologic Memory: subsequent exposures to the same antigen are faster, larger, as each exposure to an antigen generates long-lived antigen-specific memory cells, return the immune system to homeostasis faster.
Innate immune system: Fast as microbes can multiply fast, release phagocytes, inflammatory cytokines and interferons/antivirals, Cytokines.
Adaptive Immune system: takes 6-7 days.
Innate immune system recognises PAMPS and DAMPS with PPR’s
Epithelial Barrier: Physical barrier, Produce antimicrobial chemicals (direct toxicity or activation of other Leukocytes), Intraepithelial T cells recognise small number of common microbial structures (Cytokine Production and Phagocyte activation)
Phagocytes: Neutrophils and monocytes, Macrophages (recruited from blood into infected tissues in response to signals from sentinel cells).
Dendritic cells: Express many PRR, versatile sensor of PAMPS and DAMPS, capable of triggering and directing adaptive T cell mediated immune response(present In epithelia and most tissues)( uptake & transport of antigens to lymph nodes, upregulation of costimulators, production of cytokines).
Natural Killer cells: Kill infected cells via granule exocytosis of perforin and granzyme proteins adjacent to target cells, Produce Cytokine interferon (IFN)-y to increase the capacity of macrophages to kill phagocytosed bacteria.
Soluble components: recognize microbes and/or promote innate/adaptive responses
Complements: Culminate in the production of peptides that stimulate inflammation (C3a, C5a) and polymerized C6-C9 which form membrane attack complex.
cytokines: Signalling molecules that aid cell to cell communication in immune response and stimulate movement of cells toward sites of inflammation, infection and trauma.
Inflammation: Bring leukocytes and plasma proteins to the site of infection or tissue damage, eliminate the cause and initiate healing.
Inflammation symptoms: Redness, Heat , Swelling (Leakage of cells and fluid into tissues), Pain (Increased nerve sensitivity due to chemical mediators).
Inflammatory process: Offending agent recognized by host cell/molecules > produce chemical mediators, Leukocytes and plasma proteins recruited from circulation > activated to destroy and eliminate offending substance, Reaction is controlled and terminated damaged tissue repaired.
resolution of inflammation: normal permeability, Drainage of fluid & proteins into lymph, Pinocytosis into macrophages, Phagocytosis of apoptotic neutrophils, Phagocytosis of necrotic debris, Disposal of macrophages.
Type 1 Interferons: Bind onto uninfected cells inducing the expression of enzymes that block viral replication > turns on an antiviral state.
Infected cell: produce type 1 interferons that bind onto uninfected cells.