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IMMUNE SYSTEM . Innate immunity a) barrier defenses- skin and membranes (mucus, lysozyme , stomach acid, sebaceous secretions) b) phagocytosis – use TLR’s to detect foreign invaders ( monocytes (macrophages) and neutrophils and eosinophils and dendritic cells).
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IMMUNE SYSTEM • Innate immunity a) barrier defenses- skin and membranes (mucus, lysozyme, stomach acid, sebaceous secretions) b) phagocytosis– use TLR’s to detect foreign invaders (monocytes(macrophages) and neutrophilsand eosinophils and dendritic cells)
c) Peptides and proteins - interferons (innate viral replication defense), complement system (inactive proteins activated by surfaces of invaders causing lysis) • Inflammation – via histamines from basophils and mast cells (connective tissue cells) • Natural killer cells(NK) – recognize cells without class I MHC and release chemicals to kill them
Evasion by pathogens Bacterial capsules, resistance to lysozyme in lysosomes (TB bacterium)
Acquired immunity *via lymphocytes (B cells and T cells) * requires foreign antigens- invading toxins or surface markers * B and T cells have antigen receptors to recognize a small portion of an antigen, called an epitope
All antigen receptors on a single lymphocyte are identical • A single antigen can have multiple epitopes, and trigger responses from multiple lymphocytes • B cells bind to complete antigens that are free or on the surface of a pathogen • T cells bind to antigen fragments on host cells only
MHC (major histocompatibility complex) • Class I MHC- found on almost all cells (not rbc’s) - bond to foreign peptides synthesized in cells and displays them) recognized by cytotoxic T cells which kill infected cells • Class II MHC – found in dendritic cells, macrophages, and B cells- bind to engulfed foreign peptides and display them – recognized by cytotoxic T cells or helper T cells
Humoral vs. cell mediated response • Humoral response – involves the activation and clonal selection of B cells which secrete antibodies into blood and lymph • Cell mediated response – involves the activation and clonal selection of cytotoxic T cells.
Helper T cells Can play a role in both the humoral and cell mediated response • Use CD4 protein on surface to bind to class II MHC present on macrophages, dendritic cells, or B cells and then helper T cell is activated to produce cytokines. • These cytokines can activate B and cytotoxic T cells to form clones
Cytotoxic T cells Signaled into action via helper T cells or class I MHC Uses CD8 surface protein to attach to cells signaled for destruction and release cell killing proteins.
B cells B cells are activated by both exposure to an antigen and cytokines from helper T cells B cells which first encounter an antigen will ingest it and display it via Class II MHC to helper T cells Helper T and B cell direct interaction activates B cells to form clonal plasma cells
Both B plasma cells and cytotoxic T cells leave MEMORY cells behind which can last for decades (immunity)
Helper T cells also leave “clone” cells B cells can be activately independently when multiple receptors bind parts of antigens – but usually this leaves no “clone” cells
Antibody basics *closely resemble B antigen receptors (Y) Polyclonal antibodies are products of multiple B cell types, while monoclonal antibodies are the product of one type – and good for just one epitope
Antibody Functions 43.21 I. Neutralization – bind to pathogen to interfere with ability to infect II. Opsonization – bind to pathogen to mark for destruction by phagocytosis III. Complement activation – bind to pathogen to trigger complement proteins to cascade into action.
Antibodies can also bind to various hormones, toxins, etc. ( pregnancy testing, anti-venoms)
Passive vs Active immunity • Active immunity – “memory” – involves lymphocytes (immunizations, previous exposure) • Passive immunity – IgG from mother to infant , antibodies injected from outside sources
Primary immune response – first exposure takes 10-17 days to mount an attack • Secondary immune response – second exposure to same antigen – 2-7 days for attack Figure 43.15