CR1L

CR1L, formally known as Complement C1q Receptor-Like Protein, is a complement family receptor that interacts with C1q—the key initiator of the classical complement pathway. It regulates complement activation by modulating C1 complex formation, thereby influencing innate immune responses and inflammatory signaling cascades critical for pathogen clearance and immune homeostasis.
Aberrant CR1L function is linked to autoimmune disorders like systemic lupus erythematosus (SLE), where unregulated complement activity drives tissue injury. Early-stage drug development explores CR1L-targeted agents (e.g., monoclonal antibodies) to dampen excessive complement activation, holding promise for treating autoimmune and inflammatory conditions associated with complement dysregulation.