Cell mediated Immunity

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CELL MEDIATED IMMUNITY:

CELL MEDIATED IMMUNITY DR.GOGOI UNIVERSITY OF FIJI

Cell Mediated Immunity:

Cell Mediated Immunity * Host defenses against extracellular infection are mediated by: - Antibody - Complement - Macrophages * Intercellular infections are mediates by CMI * CMI are responsible for: - Resistance to intracellular pathogens - Resistance to fungal and protozoal infections - Resistance to tumors

Cell Mediated Immunity:

Cell Mediated Immunity * CMI may play a role in some harmful conditions: - Hypersensitivity reactions type IV (contact dermatitis) - Graft rejection - Autoimmune diseases * Cell mediated cytotoxicity mediated by: - T-cytotoxic cells cells - Natural killer cells - Activated macrophages

Characters Of CMI:

Characters Of CMI Cellular immune response is mediated by: - Subpopulation of T-lymphocytes - Macrophages and their products

Characters Of CMI:

Characters Of CMI * Macrophages present antigen via their surface MHC to T-cells * T-cells recognize antigen through their specific receptors (TCR) * A specific T-cell clone becomes activated and begins to proliferate * Activated TH lymphocytes becomes effectors cells that secrete cytokines

Characters Of CMI:

Characters Of CMI Cytokines stimulate other effectors cells of CMI and humoral immune response and mediate the following: - Attract monocytes, macrophages and lymphocytes to the site - Activate macrophages to kill intracellular microbes - Promote activity of CD8 CTLs which directly kill virus infected cells, tumour cells, and graft rejection - They activate NK cells increasing their cytotoxic functions - Stimulate B-cells to differentiate into plasma cells that secret antibodies

Phases Of CMI:

Phases Of CMI 1) Antigen processing and presentation Protein antigens processed and converted to peptides then bind to MHC molecules on A ntigen P resenting C ell (APCs ) to be presented to T-cells

1) Antigen Processing and Presentation:

1) Antigen Processing and Presentation a- Extracellular proteins are internalized into vesicular compartment of APCs (Dentritic, macrophages,B-cells) - They are degraded to generate peptides - These peptides bind into class II MHC molecules - Peptide-MHC II complex is transported to surface of APCs to be presented to CD4 TH cells ( T H elper cell) Outcome: Secretion of cytokines by TH cells

1) Antigen Processing and Presentation:

1) Antigen Processing and Presentation b- Endogenously synthesized proteins are degraded to peptides (all nucleated cells e.g virus infected cells) - They bind to class I MHC in endoplasmic reticulum - Peptide-MHC I complex is expressed on surface of nucleotide cells to be represented to CD8 cytotoxic cells Outcome: Killing of presenting cells by CTLs

2) Activation of T-cells:

2) Activation of T-cells * Mature CD4 and CD8 cells are activated by two signals: - First signal is recognition of antigenic peptide-MHC complex on surface of APC by TCR-CD3 complex - CD4 and CD8 molecules are co-receptors that stabilize the interaction of TH cells and TC-cells respectively with APCs - CD3,CD4, and CD8 act as signal transduction molecules - Second co-stimulatory signal is: interaction of CD28 on T-cells with CD7 on APCs

2) Activation of T-cells:

2) Activation of T-cells * TH-cells express IL-2 receptors and secrete cytokines including IL-2 * IL-2 auto activate TH-cells * APC release IL-I which acts on both APC and TH cell to promote their activation * All mentioned interactions lead to activation of mature TH-cells * Mature TH-cells proliferate and differentiate into effectors antigen specific TH-cells releasing cytokines * Some of them become memory cells which provide secondary immune response * Cytokine released from activated TH-cells activate macrophages, NK and B-cells

Phases Of CMI:

Phases Of CMI * Activated CD8 TC-cells proliferate and differentiate into a clone of effectors cells CTLs * Effectors CTLs kill target cells i.e. nucleated cells (expressing MHC-I) infected with viruses, tumor cells or graft cells

3) Activation of Macrophages and Delayed Type Hypersensitivity (DTH):

3) Activation of Macrophages and Delayed Type Hypersensitivity (DTH) * Activated TH cells (TH1) secrete IFN- γ which activates macrophages and increase their ability to kill ingested intracellular pathogens * The process of activation of macrophages, NK cell and cytotoxic T-cells, infiltration and proliferation of inflammatory cells, stimulated by cytokines released from TH-cells (TH1) is important protective mechanism against intracellular pathogen

3) Activation of Macrophages and Delayed Type Hypersensitivity (DTH):

3) Activation of Macrophages and Delayed Type Hypersensitivity (DTH) * Activated macrophages can also kill abnormal host cells (abnormal or tumor cells) * Its ctotoxicity is non specific and stimulated by TNF, nitric oxid, enzymes and oxygen metabolites * If infection is not fully resolved , activated macrophages cause tissue injury and fibrosis

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