CD200R1 regulates the severity of arthritis but has minimal impact on the adaptive immune response.

CD200R1 is a member of the immunoglobulin supergene family that is thought to play an inhibitory role in immunity. Previous studies have established the anti-arthritic effect of CD200Fc, an agonist of CD200R1. However, the physiological role played by CD200R1 in arthritis remains to be established. The aims of this study are to assess the contribution of endogenous CD200R1 in regulating the severity of arthritis and to determine its role in shaping the immune response to type II collagen within the context of collagen-induced arthritis, an animal model of rheumatoid arthritis. Arthritis was induced in DBA/1 mice by immunization with type II collagen and the kinetics of expression of CD200R1 and CD200 were monitored by quantitative reverse transcription-polymerase chain reaction. Next, a comparison was made between CD200R1(-/-) and wild-type mice in terms of the progression of collagen-induced arthritis, as well as the B and T cell responses to type II collagen. The expression of both CD200R1 and CD200 was increased after immunization and reached maximal levels at the height of the inflammatory response. In addition, the severity of arthritis was increased significantly in CD200R1(-/-) mice compared to wild-type mice. However, little or no differences were observed between CD200R1(-/-) and wild-type mice in terms of the T or B cell responses to type II collagen. It was concluded that the CD200R1/CD200 pathway is up-regulated in arthritis and plays a significant physiological role in regulating the severity of disease. In contrast, CD200R1 plays a minimal role in shaping the immune response to collagen in this model.