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Complement factor H (CFH) is a key regulatory glycoprotein in the alternative pathway of the complement system, a crucial component of innate immunity. It modulates complement activation and protects host tissues from unintended damage by competing with factor B for binding to C3b, accelerating decay of C3 convertases, and acting as a cofactor for factor I-mediated inactivation of C3b. CFH binds to polyanionic molecules on host cells, enhancing its affinity for self-tissues. Dysregulation or genetic variants in CFH are associated with diseases such as atypical hemolytic uremic syndrome (aHUS) and age-related macular degeneration (AMD).
Targets CFH would aim to modulate its activity, either enhancing it to further suppress complement activation (in diseases with CFH deficiency or dysfunction) or inhibiting it (in diseases where CFH contributes to excessive complement activation).
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