Rabbit Polyclonal CFH Antibody

The complement factor H (CFH) antibody is a critical component in the study of the complement system, a key part of innate immunity. CFH itself is a regulatory glycoprotein that inhibits the alternative complement pathway, preventing uncontrolled activation and damage to host cells. It binds to host surfaces marked by specific polyanionic markers (e.g., glycosaminoglycans) and C3b, accelerating the decay of the C3 convertase complex (C3bBb) and acting as a cofactor for C3b cleavage by factor I. Dysregulation of CFH is linked to several pathologies. Genetic mutations or autoantibodies targeting CFH disrupt its regulatory function, leading to complement overactivation. This is implicated in diseases like atypical hemolytic uremic syndrome (aHUS), where CFH dysfunction causes microvascular thrombosis, and age-related macular degeneration (AMD), where local complement activation contributes to retinal damage. CFH autoantibodies, detected in ~10% of aHUS cases, often coexist with CFH-related protein 1 (CFHR1) deletions, forming immune complexes that impair CFH activity. These antibodies are also associated with C3 glomerulopathies and other autoimmune conditions. Clinically, detecting CFH antibodies aids in diagnosing and stratifying patients, guiding therapies such as eculizumab (a complement C5 inhibitor) or plasma exchange. Research continues to explore their role in disease mechanisms and as therapeutic targets.