7. The Innate Immune System – Flashcards
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| first line of defense (3) |
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| barriers: physical, chemical and environmental, and biological |
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| first immunological line of defense |
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| innate immune system |
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| a soluble means of protection against pathogens that evade cellular contact |
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| complement system |
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| how do you know complement system is important? (3) |
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| 1. sea urchins have them 2. it develops in humans in the first trimester, 3. hereditary disorders are associated with disseminated recurrent infections |
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| complement components are made where and present where |
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| made in liver, present in blood and tissues |
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| t/f complement system only functions in the innate immune system |
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| false - also in the adaptive |
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| native complement protein components |
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| C1-9, B, D, P |
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| what component is central to all pathways |
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| C3 |
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| 3 complement activation pathways |
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| alternative, lectin, and classical |
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| C3 cleavage activates _ by what mechanism |
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| activates C5-9 via all 3 complement activation pathways |
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| opsonization (2) |
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| coats bacterial surfaces, enhancing phagocytosis. by C3b |
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| how does complement system cause inflammation |
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| stimulates histamine release (binds to mast cells and allows them to degranulate), increased blood vessel permeability, chemotactic attraction of phagocytes |
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| direct killing via complement system |
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| attach to invader, form complex, drill holes |
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| indirect killing via complement system |
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| mark invader for destruction by macrophages, attract phagocytes to the area and increase phagocytosis |
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| C3a |
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| small soluble fragment, leads to vacular increased permeability and recruitment and activation of phagocytes |
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| when is classical pathway triggered |
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| when IgM or IgG bind to antigens on microbial cell surface; Fc regions become accessible to complement proteins, and two or more Fc regions come close together |
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| C1 |
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| binding of C1q results in activation of C1r, which in turn activates C1s = activated C1qrs, an enzyme that cleaves C4 and C2 |
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| C4b |
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| binds to membrane and combines with C2b whereas C4a/C2a is released. |
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| C3 convertase |
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| C4b2b complex; C3b joins, making C5 convertase |
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| C1 esterase inhibitor |
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| C1 INH, C1 inhibitor. is a protease inhibitor that blocks the activation of C1. |
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| hereditary angioedema |
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| tissue swelling that looks like allergic reaction, caused by deficiency of C1-INH |
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| MBL pathway |
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| lectin pathway=mannose-binding lectin pathway. MBL+mannan+MASP1and2>complex>activation of the MASPs and cleavage of C4 and C2 |
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| lectin |
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| protein that is able to bind to a carbohydrate molecule found at surface of common pathogens (innate) |
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| MBL / produced/stored where |
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| a protein that specifically binds to mannans (mannose-containing polysaccharides, found on surfaces of bacteria). produced in liver, found in blood and tissues |
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| binding of MBL to a pathogen results in |
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| the physical association of two MBL-associated serine proteases (MASPs). MASP1=C1r, 2=C1s, MBL=C1q |
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| alternative pathway / technical |
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| also innate, unlike classical. natural breakdown of plasma C3 via spontaneous cleavage of the highly reactive thioester bond (now located on C3b) allows C3 to attach to any nearby host or foreign surface unless that surface is protected. / C3b+B > C3bBbP (this is C3 convertase and that reaction happened through the catalyst D) > C3bBb3bP (this is C5 convertase) |
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| how to regulatory proteins on host cells protect them |
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| by inactivating C3b |
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| t/f spontaneous cleavage is the only innate way to cleave C3 |
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| false - a variety of enzymes also do it |
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| C3b can bind to _ because it's very reactive (2) |
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| amino or hydroxyl groups; many bacterial cell walls have these |
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| if C3b doesn't react with anything in 60 microseconds |
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| it is neutralized by water |
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| alternative pathway C3 convertase is stabilized by |
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| properdin = factor P |
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| DAF |
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| decay accelerating factor = a protein on the surface of human cells that accelerates breakdown of the convertase C3bBb by other proteins in the blood (decays complement) |
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| CD59 |
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| human cell surface protein that kicks "almost finished" MACs off before they can make holes |
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| "grenade" |
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| C3b |
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| complement regulatory proteins |
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| are present on human cells but not microbial cells |
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| terminal complement inhibitor proteins |
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| are anchored to RBC surface by GPI tails; are crucial in protecting blood cells from inappropriate destruction. |
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| PNH / symptoms |
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| paroxysmal nocturnal hemoglobinuria: disease caused by lack of host cell protection from complement / anemia, fatigue, dark colored urine |
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| "smart bombs" |
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| lectin activation pathway |
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| phagocytes |
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| eat invader + fuse with lysosome to destroy invader. produce cytokines that call more leukocytes into the area, inducing inflammation |
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| how does the innate immune system know what to kill? |
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| PAMPs (pathogen associated molecular patterns), using a limited number of PRRs or pattern recognition receptors |
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| PAMPs / 2 examples |
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| sugars, NAs, lipids, proteins or combos of any of these; widely expressed on viruses and bacteria. / bacterial LPS (lipopolysaccharide) on gram-negative bacteria, peptidoglycans on gram-positive |
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| Toll-like receptors |
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| TLRs mediate recognition of diverse pathogens. after binding to PAMPs > enhanced activation of genes encoding cytokines in the nucleus of the invader (and other molecules involved in antimicrobial activity). result: synthesis and secretion of cytokines that promote inflammation and the recruitment of leukocytes to the site of infection |
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| NK / how do they kill |
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| kills virus and cancer. functions in production of cytokines. / insertion of perforin and granzymes |
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| MHC I |
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| molecules sending a "kill" signal to CTLs. NK cells however kill based on absence of a "don't kill" signal as well as presence of a "kill" signal |
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| neutrophil |
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| = part of the innate system, multi-lobar nucleus |
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| lymphocyte |
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| adaptive, big round nucleus |
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| major players of adaptive immune system |
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| B, T, and APC |
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| T lymphocytes |
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| CD8 (CTL) and CD4 (T helpers: Th1 = CMI, Th2 = Humoral) |
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| physical barriers |
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| skin, mucous, cilia |
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| chemical and environmental barriers |
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| sweat, stomach and vagina acids; digestive enzymes; microbicidal substances on skin and mucous |
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| biological barriers |
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| =commensal organisms: skin, GI tract, vagina |
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| innate immunity |
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| complement, NK, phagocytes (neutrophils and macrophages) |
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| sequential activation |
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| of complement components results in release of fragments important in inflammation and in formation of MAC |
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| lytic pathway |
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| =terminal pathway, = attachment of C5b to the bacterial membranes leads to the addition of components C6, C7, and C8. this facilitates addition of multiple C9 molecules to form a pore in the membrane |
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| what does C1 INH inactivate other than C1 |
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| fibrinolytic, clotting and kinin pathways |
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| "pigtail" |
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| =GPI tail on RBCs that binds to DAF to protect against complement. deficiency = PNH. |
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| CTLs kill by same mechanism as _, but |
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| NK, but CTL is adaptive instead of innate |
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| expression of MHC-I molecules is often _ by virus/cancer, = _ |
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| depressed / loss of don't kill signal |
