Studying tonight

Just a little insight into how I have spent the last hour of my life...

-Antibody binds antigen
-C1q binds Fc of antibody
-C1r and C1s are recruited and complex with C1q
-this complex cleaves C4, C4b stays and binds while C4a leaves
-C1q1r1s also cleaves C2, C2a stays and binds while C2b leaves
-C4b2a (classical C3 convertase) cleaves C3, C3b stays and binds while C3a leaves
-C3b can lead to phagocytosis of pathogen... OR
-Factor B and bind C3b, Factor D cleaves Factor B, and leaves C3bBb
-C3bBb (alternative C3 convertase) cleaves more C3, keeping C3b to perpetuate cycle
-C3a (and other small molecules that have left) act to recruit inflammatory cells
-C4b2a3b (C5 convertase) can cleave C5, C5b stays and C5a leaves
-C5b recruits C6, C7, C8, and C9... these lead to perforated holes in the antigen surface... which leads to death
-C1INH is the inhibitor that prevents C1 complex, thus complement cascade is stopped
-C4BP binds C4b, preventing C4b2a from forming... free C4b is inactivated by Factor I
-Factor H binds C3b, allowing it to be cleaved by Factor I
-these all prevent complement from overrunning our cells
-DAF and MCP both protect our own cells by preventing complement activation