Rheumatoid arthritis (RA) is an autoimmune inflammatory disease exhibited most commonly in joints. We found that the expression of C1qtnf3, which encodes C1q/TNF-related protein 3 (CTRP3), was highly increased in two mouse RA models with different etiology. To elucidate the pathogenic roles of CTRP3 in the development of arthritis, we generated C1qtnf3-/- mice and examined the development of collagen-induced arthritis in these mice. We found that the incidence and severity score was higher in C1qtnf3-/- mice compared with wild-type (WT) mice. Histopathology of the joints was also more severe in C1qtnf3-/- mice. The levels of antibodies against type II collagen and pro-inflammatory cytokine mRNAs in C1qtnf3-/- mice were higher than WT mice. These observations indicate that CTRP3 plays an important role in the development of autoimmune arthritis, suggesting CTRP3 as a possible medicine to treat RA.
|ジャーナル||Biochemical and Biophysical Research Communications|
|出版ステータス||Published - 2014 1 3|
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology