| First Author | Li J | Year | 2013 |
| Journal | Proc Natl Acad Sci U S A | Volume | 110 |
| Issue | 18 | Pages | 7395-400 |
| PubMed ID | 23589893 | Mgi Jnum | J:196663 |
| Mgi Id | MGI:5489002 | Doi | 10.1073/pnas.1221608110 |
| Citation | Li J, et al. (2013) Deficiency of beta-arrestin1 ameliorates collagen-induced arthritis with impaired TH17 cell differentiation. Proc Natl Acad Sci U S A 110(18):7395-400 |
| abstractText | Rheumatoid arthritis (RA) is an inflammatory disease in which interleukin 17 (IL-17)-producing T helper 17 (TH17) cells have been critically involved. We show that in patients with RA, the expression of a multifunctional regulator beta-arrestin1 was significantly up-regulated in peripheral and synovial CD4(+) T cells, which correlated well with active phases of RA. In collagen-induced arthritis, deficiency of beta-arrestin1 ameliorated disease with decreased TH17 cell differentiation, proinflammatory cytokine production, synovitis, and cartilage and bone destruction. Further mechanistic study reveals that beta-arrestin1 promoted signal transducer and activator of transcription 3 (STAT3) activation required for TH17 cell differentiation through scaffolding the interaction of Janus kinase 1 and STAT3. These findings indicate a critical role for beta-arrestin1 in the pathogenesis of collagen-induced arthritis and TH17 cell differentiation and suggest beta-arrestin1 as a potential diagnostic biomarker and therapeutic target for RA. |
