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24 Cards in this Set

  • Front
  • Back
ring leader of the cytokines
CD4 Tcell
what would disappear if you lost the CD4 T cells
IL-2, 4,5, decrease in INF-gamma, decrease B cells, CD8 T cells, NK cells, monocytes, and macrophages (which stimulate CD4-Tcells so you are really f-ed)
Relate Bradykinin and ACE-I
ACE-I inhibits ACE, which inhibits Bradykinin, so with ACE gone, Bradykinin increases and causes exudation, pain, and vasodilation (which is why ACE-I are antihypertensive drugs)
what cell is affected in HIV
CD4 Tcells
region on chromosome 6
only on nucleated cells surfaces
HLA class I
present on antigen presenting cells
HLA class II
presents foreign substance that have been phagocytosed by antigen presenting cells
HLA class II (the docking antigen)
what do macs, T cells, B cells, and granulocytes (-phils) have in common
all release INF-alpha for anti-viral affects (induce MHC-1 and inhibit mRNA translation of virus)
what interleukon stimulates B cells that is not from the T cell?
IL-7 (from bone marrow), also stimulates T cells (which is why it cant come from T cells)
how is the fibroblast related to T, B cells, macs, and granulocytees
it is anti-viral too BUT with release of INF beta & it is related to the T-cell because it releases IL-6 to stimulate B cells
PDGF comes from what cells
platelets and endothelial cells
IL-1, IL-6, and TNF-alpha are all related how?
they stimlate the ACUTE phase response of the immune system
why would you monitor CRP in a pt with chronic immune disease
it measures the stage of the disease (exacerbation or regression phase) increase in CRP = exacerbation and decrease in CRP means Sx will start regress
what pathway is started by endotoxins
what pathways is started by antibody-antigen complexes
what are the two convertases of C3
4b2b (classical) and 3bBb (alternate)
related 5a and 3a to shock (decrease blood pressure)
if the complement pathway is activated, 3a and 5a are eventually released, they stimulate histamine, and histamine decrease the BP by vasodilation (ie: endotoxin can cause septic shock this way)
how does C5a mediate inflammation
chemotaxis (1.1)
how does C3b mediate inflammation
opsonization (1.1)