Chapter 2 & 3 - Innate Immunity Flashcards
What are the roles of:
- C3a
- C3b
- C5-9
- C3a = a chemoattractant for neutrophils and macrophages; attracts phagocytes to pathogen’s surface (recruitment of inflammatory cells)
- C3b = covalently bound to pathogen (complement fixation), tagging the pathogen for destruction by phagocytes; also involved in formation of more C3 convert axe
- C5-9 = perforation of pathogen cell membranes
Complement
A system of plasma proteins that mark pathogens for destruction
Define the 3 pathways of complement activation in the order in which they act.
1) Alternative Pathway = pathogen surface creates local environment conducive to complement activation
2) Lectin Pathway = mannose-binding Lectin binds to pathogen surface
3) Classical Pathway = C-reactive protein or antibody binds to specific antigen on pathogen surface
Properdin
- factor P
- increases the speed and power of the complement activation by binding to the C3 convert are (C3bBb) on microbial surfaces and preventing its degradation by proteases.
Factor B & D
- Take part in formation of the C3 convertase
- hydrolyzed C3 binds factor B, which is cleaved by factor D to make C3 convertase
Factor H and I
- opposite of Properdin
- factor H binds to C3b and facilitates further cleavage to a form called iC3b by the protease Factor I
- needed so that the reservoir of C3 in the blood, lymph, and EC fluid is not depleted
DAF and MCP
They both disrupt C3 convertase on human cell surface so that it is not destroyed.
- DAF = decay-accelerating factor; binds to the C3b component of the alternative C3 convertase, causing its dissociation and inactivation.
- MCP = membrane cofactor protein; binding of MCP to C3 convertase makes the convertase susceptible to cleavage and inactivation by Factor I (similar to Factor H)
CR1
The complement receptor on macrophages that binds to C3b on bacterium cause endocytosis of bacterium for phagocytosis.
Membrane Attack Complex
- C5-9
