Complement system component

The complement system is a complex network comprising more than 30 plasma proteins that play a central role in innate immunity. These proteins circulate mainly as inactive precursors until activated by one or more triggers—pathogen surfaces via pattern recognition molecules or antigen–antibody complexes. Activation occurs through three main pathways: classical pathway triggered by antigen–antibody complexes involving IgG/IgM binding to C1q; lectin pathway initiated by mannose-binding lectin binding microbial carbohydrates; and alternative pathway driven by spontaneous hydrolysis ("tick-over") and stabilization on pathogen surfaces. Upon activation via any pathway, a proteolytic cascade ensues leading to opsonization with fragments like C3b/C4b tagging pathogens for phagocytosis. The release of anaphylatoxins such as C3a and especially C5a induces inflammation and recruits immune cells. Ultimately the terminal sequence forms the membrane attack complex causing lysis primarily on Gram-negative bacteria but also on host cells if not properly regulated. The system is tightly controlled by soluble inhibitors like Factor H/I/CD59/DAF/protectin which prevent inappropriate activation against host tissue while allowing robust responses against pathogens. Dysregulation can lead either toward immunodeficiency/increased infection risk when deficient—or toward excessive inflammation/tissue damage when overactive—contributing significantly both directly through effector functions but also indirectly through crosstalk with adaptive immunity.[1][2][6]

Other names

Complement cascade proteinscomplement factorscomplement pathway proteins

Inhibition of complement activation at various points in the cascade; Blockade of terminal pathway to prevent membrane attack complex formation; Inhibition of anaphylatoxin receptors to reduce inflammation; Enhancement or modulation of regulatory pathways