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Complement C1q subcomponent subunit A (C1QA) is one of three polypeptide chains (A, B, C) forming the C1q molecule, the recognition protein of the classical complement pathway of the innate immune system[2][3][4]. C1q, together with C1r and C1s, forms the C1 complex that binds to antigen-antibody complexes, initiating the classical complement cascade and amplifying immune responses[3][4][5]. C1q is referred to as a pattern recognition molecule for its ability to bind various ligands, such as immunoglobulins, apoptotic cell surfaces, and microbial components, thereby mediating immune complex clearance and modulating inflammation, apoptosis, angiogenesis, and synaptic pruning in the central nervous system[1][2][4]. The C1QA chain contributes to the collagen-like region and the globular domain of the C1q molecule, which is essential for binding to pathogens, immune complexes, or cell debris[1]. Deficiency or dysfunction of C1q or its subunits is strongly associated with severe autoimmune diseases like systemic lupus erythematosus (SLE), glomerulonephritis, and has roles in neurodegenerative and cardiovascular disease[2][3][5]. Current therapies indirectly modulate C1q activity but direct C1QA-targeting drugs remain experimental.
Inhibition of complement activation (via classical pathway blockade); antibody binding to inhibit or modulate C1q-mediated immune complex clearance; modulation of inflammatory, phagocytic, or immune tolerance pathways
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