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Immunology (Adaptive Immunity (B Cells (The receptor ; 2 kinds of proteins…

- - - - Non-specific cell response once gotten past first level surface chemical/barrier protection
        
        Second line of defense
        
        Natural Killer cells
        
        Killer - cell suicide response
        
        Cell signaller -Cytokines
        
        uses "roll, stop exit" to leave blood can kill tumor cells, virus infected cells, bacteria, parasites and funghi
        
        Nk cells employ an injection mechanism which uses perforin protein to deliver suicide enzymes to target cell (granzyme B)
        
        Fas ligand interacts with Fas on target cell surface signalling the cell to commit suicide
        -IFN-y = more effective killer
        
        Macrophages
        
        Cell signaller- Cytokines
        
        IL-1 and TNF produce cytokines facilitate communication between cells of immune system
        cytokines ; part 1 alert macrophages to bacterial attack
        part 2 signal to other immune system cels travelling in nearby capillaries and influence them to leave the blood and help with the fight
        Inflammatory response
        
        Garbage collectors
        
        Phagocytosis - phagosome and lymphocytes
        
        Antigen Presenting Cells (APCs)
        
        Class I - endogenous proteins this has been manufactured by the cells for killer t cells to inspect
        
        Class II - exogenous digested proteins present invaders that have been phagocytksed helper t cels can inspect these and then signal other cells to help
        
        Major histocompatibility complex (MHC) cell surface signal presenter
        
        NEUTROPHILS
        
        ~70 of white blood cells in circulation 5 day lifespan die by committing suicide (apoptosis) NOT APC as they exit blood (extravasation) they are activated similar to hyper activated macrophage "roll, stop exit" mechanism to leave blood
        
        immature= monocytes 2x102 in blood
        
        Complement Proteins
        
        Membrane attack complex (MAC)
        
        This is what is presented/ formed on pathogenic bacterial cells terminal complement complex hole in cell wall allows lysis
        
        Cell signaller - C3b
        
        overview
        
        ~ 30 different proteins ~ originated in sea urchins 700 million years ago
        ~ formed in 1st trimester of development ready to go from birth
        
        2nd main pathway: The classical pathway (depends on antibodies
        
        3rd (not main) pathway lectin activation pathway
        
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        1st main pathway: the alternative pathway
        
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        stops from attacking own cells
        Regulators of complement activation (RCAs) one of which Decay Accelerating Factor (DAF) accelerates the breakdown of c3bBb by other proteins in the blood
        
        CD59 can 'kick off' MAC (membrane attack complexes) before they can make a hole in cell surface
        
        opsonisation complement marks the bacterial invader for phagocytosis
        
        A co-operative effort
        
        Infected cell binds to NK cell = IFN-y acts on macrophage which produces Il-12 which increases amount of IFN-y produced by NK cells and in turn primes more macrophages
        
        Professional phagocytes and complement system;
        
        complement fragment C3b tags invaders for phagocyte digestion
        
        C3b can bind to receptors on macrophage and provide an activation signal in a similar way to that of LPS
        
        activated macrophages in turn produce many proteins- C3, factors B and factors D #
        
        first line of defense
        
        Physical (skin 2m2)
        
        Chemical (mucous membranes: digestive tract, tears (lactoferrin) sebum, reproductive tract
        
        Flora - beneficial microbes living on our skin
- - - - Cell signaller - cytokines
      - Mark cells for destruction
      - CD4+ =MHC II
    - - CD8+ = MHC I
      - Killers
      - Activation
        
        TCR identify target adhesion molecules on killer cell then uses perforin to attack similar to C9 complex once attached delivers a mixture of perforin and granzyme B
    - - Antigen Presenting Cells
        
        activated dendritic cells
        
        Toll like receptors -TLR-4 gram negative bacteria LPS -TLR-2 gram positive bacteria
        TLR-3 recognises ds RNA produced during viral infections
        TLR-9 recognises unmethylated DNA (CpG_ characteristic of bacterial DNA
        (also detect heat shock proteins)
        important as they initiate immune response by activating virgin T cells; does this by migrating to lymphatic system and upregulating MHC II and costimulatroy B7
        
        activated macrophages
        
        Cant travel so; differ to DC macrophages constantly restimulate T cells to stop them from dying or entering resting state
        
        activated B cells
        
        increase levels of MHC II and B7 dramatically can then act as APC for Th cells (advantage is ability to concentrate antigen for presentation)
        
        Helper T cell activated
        
        Naive cells upon activation receptors appear and IL-2 is unregulated don't have IL-2 receptors clonal selection because only those properly activated Th cells will produce the growth factor receptors which allows for proliferation and produces many clones
        
        Single Th cells don't produce all cytokines, will produce a subset of them.
        
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        How do Th cell know what cytokines to secrete?
        
        Where in the body they are invaded
        
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        Recognise what invader dealing with, bacterium, virus or parasite
        
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        Once activated and proliferated Th cell becomes effector helper T cell
        
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    - - career choice
        
        T cells programmed to due in whats called activation induced cell death (ACID)
        
        Some kept for memory cells just like Bcells
  - - - Antigen that BCR recognises is called a COGNATE antigen ~ actually binds 6-12 amino acids called epitope
        once bound signals nucleus of B cell so that genes involved in activation can be switched on or off.
        via accessory proteins Iga and IgB which associate with the Hc protein
      - by clustering or cross linking for B cell activation
      - B cell receptors can recognise complement tag iC3b cross linking complement and bcr amplifying signal this is called co-receptor
      - never encountered antigen = virgin/naive vs. have encountered are experienced
        
        activation of naive: 2 signals: clustering of BCR and a second co stimulatory signal from helper T cellCD40-CD40L receptor
        
        activation of experienced; less stringent stimulates when meet antigen again produce new protein on surface eg. IL-2 which stimulates B cells to proliferate.
        
        Clonal selection: B cells recognised cognate antigen thus activated will react to growth factors like IL-2 and proliferate to form clones with identical BCRS
    - - Class switching - B cell can change class of antibody it produces
        
        IgM
        
        First class to evolve, can fix 10 c1 complexes known as fixing complement
        
        Whats the difference between an opsonizer and a complement fixer? Ask fiona.
        
        IgG; antibody passed from mother to fetus
        
        IgG1; binds to invaders to opsonise them for phagocytes
        
        IgG3; bind by bridge and Fab region to Nk cells increase efficiency antibody-dependant-cellular-cytototoxity (ADCC)
        
        cytokines from T helper cells causes class switching
        
        TGF-B = switch to IgA
        
        IFN-y = switch IgG3
        
        IL-4 IL-5 = switch to IgE
        
        IgE
        
        usually on mast cells to destroy , granules in mast cells usually histamine : main driver of allergic reaction as build up of IgE cause unpregnated degranulation in extremes causes anaphylactic shock
        
        IgA
        
        more IgA than any other antibody as it guards the mucosal surfaces of the body
        clipped tail structure allows passage into intestine
        acts by coating pathogens secreted in mothers milk
      - Career choice; decides whether to be antibody factory (plasma cell) or Memory B cell
        
        Plasma cell ~2000 antibodies/seconds travel to spleen of been marrow
        
        High affinity BCR present as memory cell so able to respond quick to low levels of antigen in infection
- - - - for research can be prepared in rabbit/sheep purified at end by affinity chromatography
  - - - Chrones disease