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Hypersensitivity, People have genetic predisposition to have over…

- - - - 1) MAC (membrane attack complex) = complement system C5b, C6-C8 and C9
        2) MAC "attack" the cell by inserting itself into cell mb creating a channel
        3) Osmotic diff, fluid rushes into the cell => swells, lysis, dies
    - - 1) IgG antibodies coat a blood cell and are bound by C3b
        2) Opsonized, targeted and destroyed by macrophages and neutrophils
    - - Activation of the complement system (complement proteins) by IgG or IgM
        
        Kill RBC bound to penicillin (and IgG/IgM)
        
        1) C1 (complement protein) binds Fc portion of the antibody (IgG/IgM)
        2) C1 engages C2 through C9 (activated by cleavage)
        3) Cleaved fragments C3a and C5a = chemotactic factors = attract neutrophils
        4) Neutrophils release: Peroxidase (oxygen radicals cytotoxic for cells = tissue damage)
        5) Drug reaction (penicillin) = Hemolytic anemia, thrombocytopenia, neutropenia
    - - Antibody- dependent cell-mediated cytotoxicity (ADCC)
        
        1) Antibody-complex gets recognized by Natural killer cells
        2) NK cells recognizes Fc tail of the antibody and release toxic granules
        3) Granules contains: Perforins = pores in the cell
        4)This time the pore allows entry of enzymes = Cell death in apoptotic manner = no inflammation
- - - - DNA autoantigen get released from damaged cell
        
        Circulating B cell bind to it and T cell will bind to B cell to recognize the antigens, help B cell to differentiate into IgG
        
        Lot of antigens relative to the number of antibodies bc DNA is in most cells
        
        Small complex = Less immunogenic = Less attractive = Less remove from the blood as quickly
        
        They find a way into basement mb layer of various blood vessels
        
        Once here, immune complexes activate complement system
        
        C1 bind to the antibody -> chain reaction activate C2-C9
        
        When complement P activated its cleaved by an enzyme = C3a, C4a, C5a = anaphylatoxins = increase vascular permeability
        
        Edema
        
        Complement used in large amount (C3,C4) instead of type II
        
        Chemokines attraie neutrophils = degranulates lysosomal enzymes, ROS = Vasculitis
      - Kidneys = glomerulonephritis
        
        Joints = arthritis
  - - - Foreign serum -> antibody response
- - - - 1) Person breathe pollen
        2) Antigen presenting cells (macrophages, dendritic cells) bring antigens to lymph nodes and present it to (naive) T-helper cells (can bind to a specific molecule on the pollen )
        
        When the person is allergic
        
        Antigen-presenting cell express costimulatory molecules
        
        T-helper + antigen + costimulatory molecule = type 2 T-helper cell
        
        T-helper -> TH2 thanks to cytokines:
        
        interleukin 4, 5 and 10
        
        TH2 release interleukin 4 and attract B cells:
        
        Antibody class-switching= B cell switches from making IgM antibodies to making IgE antibodies
        
        IgE antibodies have a high affinity for receptors on mast cells = ready for action
        
        TH2 cells release interleukin 5:
        
        Stimulate product° and activat° of eosinophils
        
        degranulates and releases a whole bunch of toxic substances that can damage both invading cells and nearby host cells
    - - 1) She breathe pollen again
        2) Sensitive mast cells use their coat of antibodies and binds to antigens
        3) IgE antibodies signals mast cell to degranulate and release pro-inflammatory molecules = Mediators
        
        Major mediators released in allergic reaction = Hitamine
        
        Histamine binds to H1 receptors and cause:
        
        Smooth muscle around the bronchi to contract
        
        Airways get smaller making it more difficult to breathe
        
        Blood vessel dilatation and increased permeability of the blood vessel walls = EDEMA, SWELLING, urticaria or hives
        
        Mast cells release pro-inflammatory mediators = activate eosinophils and proteases
        
        More immune cells like TH2 cells, eosinophils, basophils are recruited to the site where allergen is located:
        
        Interleukin 4,5, 10
        
        Leukotrienes (LTB4, LCT4) -> attract immune cell (neutrophils, mast cells, eosinophils)
        
        Anaphylactic shock =
        
        Increased vascular permeability + constriction of airways can be severe enough such that the body can’t supply the vital organs—like the brain, with enough oxygen- rich blood