Description
C1q, a key player in the classical complement pathway, seamlessly bridges innate and adaptive immunity. As part of the C1 complex, along with C1r and C1s, it activates upon binding to antibody-antigen complexes. This vital function positions C1q as an essential mediator in immune response management. Beyond activation, C1q recognizes IgG or IgM antibodies, initiating classical pathway activation through critical conformational changes. Its ability to bind apoptotic cells enhances immune clearance, preventing overstimulation. Predominantly produced by macrophages and dendritic cells, C1q is pivotal in maintaining host defense and preventing autoimmune diseases like systemic lupus erythematosus (SLE). C1q deficiencies, whether genetic or from anti-C1q antibodies, impair apoptotic cell clearance, heightening SLE risk. This correlation is evident in conditions like proliferative glomerulonephritis and SLE flares, where C1q levels are notably low. The C1QA gene polymorphism, associated with reduced C1q levels, highlights its integral role in immune regulation. C1q's significance extends to its diagnostic potential in understanding complex immune diseases, making it a vital biomarker in immunological research.