In this study, by generating C1qtnf6−/− and Tg mice, we demonstrate that CTRP6 is a novel regulator of the complement AP and plays important roles in the maintenance of pregnancy and the pathogenesis of disease models such as collagen-induced arthritis (CIA)22, anti-collagen antibody-induced arthritis (CAIA)6, experimental autoimmune encephalomyelitis (EAE)23 and Arthus reaction24. This evidence concerns the gene C1QTNF6 and experimental autoimmune encephalomyelitis.