Complement/Humoral Flashcards
neutralize microbes and microbial toxins
IgM, IgG, IgA - bind viruses and prevent attachment to cells; binds toxins and prevent toxin from binding receptors on cells
opsonophagocytosis
IgM, IgG - coat microbe which then bind to macrohpages and neutrophils via Fc-gamma-R or complement receptors
induces phagocytosis, ROS, NO, proteolytic enzymes
major mechanism for encapsulated bacteria - spleen is the major site for phagocytosis
complement: C3b, C4b, iC3b, iC4b
antibody-dependent cellular cytotoxicity
IgG - once bound to antigen, binds to Fc-gamma-R on NK cells; NK cells then release perforin and Granzyme B
eosinophil/mast cell
IgE binds to Fc-epsilon-R which causes the eosinophils and mast cells degranulate
different from the others because IgE does not bind to the antibody
complement
IgM, IgG
protect mucosal surfaces
IgM, IgA - IgA production is induced by TGF-B which is produced in mucosal-associated lymphoid issue (MALT)
protect neonates
IgG binds FcRn, which transports IgG across placenta
M cells
transport antigens from lumen into Peyer’s patch (small lymph node)
alternative pathway of complement activation
either spontaneous C3 hydrolysis to get C3b or get C3b from classical/lectin pathway -> C3b + microbial charged surfaces -> add factor B to get C3bB -> factor B cleaved by factor D -> C3bBb -> add factor P to get a C3 convertase: C3bBbP -> can get C5 convertase by adding C3b to C3bBb
lysis of cell membranes
neisseria: Mac complex
inflammation
chemotaxis (neutrophils): C5a»_space; C5b67
mast cell degranulation: C5a»_space; C3a, C4a (anaphylatoxins)
solubilizaiton and clearance of immune complexes from circulation
C3b, iC3b
B lymphocyte co-activation
C3d
opsonic and adhesion complement receptors
CR3, CR4 > CR1 (phagocytes)
anaphylaxis
C5aR > C3a/4aR (mast cells, basophils and smooth muscle cells)