Immunology 2

rpbardoul
Mind Map by rpbardoul, updated more than 1 year ago
rpbardoul
Created by rpbardoul over 6 years ago
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Immunology

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Immunology 2
  1. The complement system
    1. Innate
      1. Lectin Pathway: MBL (a recpetor) binds to Mannose residues on the cell surface of bacteria. The subsequent MAPS-2 allows C3 convertase reaction to occur
        1. Alternate pathway- In non infected cells SALIC acid allows for the rapid destruction of C3b which circulates in low levels. In infected state the antigen will bind with C3B as will Factor D, B and properidin to form C3 Convertase
          1. The terminal pathway is the same for all... The Anaphylotoxins (a)- C3a and c5a will bind to MAST cells and promote vasodilation. The c5b activation is the patform of cascades to form a polymer- The MAC attack (membrane attack complex) product allows for cell lesion/destruction
        2. Acquired
          1. The classial pathway:The is when a single IGM or two adjacent IGG bind to a C1 and alow subsequent c2-C4 cleavage to occu.The product is C3 CONVERTASE
          2. A group of 25-30 proteins (lettered and numbered) that are synthesized in the LIVER. Membrane damage,immune adherance and opsonization. This also promotes chemotaxis and chemokines
          3. Viral Infections
            1. Innate immunity: Anatomical, Physiological, Phagocytic and Inflammatory
              1. NK cells: These are cyttoxic to virally infected cells, crucial in the first 1-2days. They are able to recognise and destroy "mutated MHC 1's"
                1. Interferons: These activate neighbouring cells- they enhance the acquired immune response via ^ expression of MHC 1/2
                2. Acquired Immunity
                  1. Humoral *TH2: Theappropriae release of cytokines allow for B cell clonal selection. Production peaks 2-3 w after initial infection
                    1. Antibodies do not break down cells, they BLOCK the BINDING of the virus to the HOST cell
                      1. IgM, IgA and IgG
                      2. Opsonise for phagocytosis
                        1. IgM and IgG
                        2. Agglutination of cells
                          1. IgM (the primary response)
                          2. Cell Mediated Immunity *TH1:
                            1. Cytotoxic T cells are MHC restricted but they are able to lyse virally infected cells. Macs are often the professional APC's to TH cells and also aid in phagocytosis
                              1. There are certain cytotinx (IFN-gamma) which is released to DIRECT antiviral activity
                                1. NK cells can destroy via ADCC and non specifically
                            2. BOTH CMI and Humoral are key
                            3. Intracellular Bacteria
                              1. The TH1- cyto0toxic response is the most important
                                1. LISTERIA: This is a facultative anaerobe that is widely distributed in the env. It may penetrate the GIT and cause spleenic and hepatic division. = Abortion, septicaemia and meningitis
                                  1. Evades the immune system via production of LYSIN, the lysosome is destroyed- does not form and the bacteria gains access to the cytoplasm. After replication the pathogen travels to the periphery (filaments) and enter adjacent cells via membrane projections (never exposed)
                                    1. Macs are activated- TNF is then released which allows NK cells to produce IFN . These macs also promote the direct dstruction of infx hepatocytsThe release of INTERFERON Y from NK cells is crucial to supportive macrophage activation and death of bacteria. Once the infection is controlled, 1L-10 will down regulate the response.
                                  2. There is activation of alveolar macs. These are professional APC'S which activate TH cells, release of interferon sways acquired immunity predmoninantly towards CYTOTOXIC (TH1). A primary tubercle attacked my macs is suported by cytotoxic T cells
                                    1. These evade the immune system by hiding in the "cornerstones" where they cannot be attacked by" Macs, antibodies and the Complement system. They are mobile and rapid dissemination occurs. They PREVENT the lysosome bind and bacteria can then escape into the cytoplasm. They NOW produce a "LETHAL HIT", necrosis and rapid spread
                                      1. Mycobacterium TB: A few pathogen enter the bronchi (resp tract)
                                      2. A TUBERCLE forms in infected tissue (lungs, LN)- calcified and radio-opaque. This is a combination of macs and actuvated T cells. It is the site of infection, protection, persistance and pathology. It can become re-activated
                                  3. Extracellular Bacteria
                                    1. TH2 antibody productionis the main response but there are essentially four methods... This icludes the CLOSTRIDIAL disease- Tetani, Boltulium, Bacillus and ENTERObactericae- Yersninia, Klebsiella etc
                                      1. Neutralisation by enzymes or antibodes
                                        1. Death by complement, Ig and lysosomes
                                          1. Opsonisation by antibodies, collectins and complement (C3b)
                                            1. Phagocytosis and Intracellular destruction by Macs
                                            2. Innate immunity
                                              1. Enzymes, Iron binding proteins (transferin and lactoferin), defensins, interferons and the complement cascade...
                                              2. Acquired Immunity
                                                1. Opsonization of encapsulated bacteria allows phagocytosis- bind the Fc fragment (string on soap) Opsonisation can occur via; 1) Collectins which recognise foreign C3b and 2) Anti-bodies and C3b comps- phagocytes have a receptor for C3b!
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