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Final Exam Review.pdf - Final Exam Review Thursday December...

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Chapter 1 -Commensal bacteria, microbiota, antibiotics kill off good microbiota which give rise to opportunistic pathogens such as C. Diffisil -Mechanical & chemical barriers to infection, immunological barriers -Complement tags pathogens -Inflammation recruits WBCs to site of infection, innate cells create pro-inflammatory conditions -Cytokines carry messages -Toll-like Receptors cause activation of innate cells by recognizing pathogen -Clonal selection: naive lymphocyte selected to fight against pathogen -Hematopoiesis & all of the cells with their functions -Lymphoid tissues (know difference between primary and secondary) -Spleen gives adaptive immunity to blood infections (asplenia) Chapter 2 -Complement system: 30 diff serum proteins -C3b tags pathogen, C3a & C5a, C5b makes holes in surface of cell -3 outcomes of complement: lysis, recruitment of inflamm cells, opsonization (facilitate phagocytosis) -classical pathway activated in presence of C-reactive protein & during presence of antibodies -all converge at cleavage of C3 into C3a & C3b; C3a is recruitment factor, C3b opsonization, C5b initiates MAC -alternative C convertase (C3bBb) -C5b initiates MAC, C5a induces anaphylactic shock -C reactive protein initiates classical pathway -C3b is most important, if did not have, would be susceptible to infections -3 pathways of complement: alternative (innate - first to act), lectin (innate - second) & classical pathway (innate & adaptive - third) -pathogen recognition domain -TLR4 (macrophages) recognizing LPS -TLRs also inside of cell (TLR3 for example) -TLR4 signaling leads to activation of TF NFkB & synthesis of inflamm cytokies; NFkB activates cytokine genes; inability to activate NFkB = NEMO -Pro-inflamm cytokines: IL-1beta (fever producer), TNF-alpha (vasodilator), IL-6 (induce
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