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- W2016688255 abstract "Rheumatoid arthritis (RA) is an inflammatory disease in which interleukin 17 (IL-17)-producing T helper 17 (T(H)17) cells have been critically involved. We show that in patients with RA, the expression of a multifunctional regulator β-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 β-arrestin1 ameliorated disease with decreased T(H)17 cell differentiation, proinflammatory cytokine production, synovitis, and cartilage and bone destruction. Further mechanistic study reveals that β-arrestin1 promoted signal transducer and activator of transcription 3 (STAT3) activation required for T(H)17 cell differentiation through scaffolding the interaction of Janus kinase 1 and STAT3. These findings indicate a critical role for β-arrestin1 in the pathogenesis of collagen-induced arthritis and T(H)17 cell differentiation and suggest β-arrestin1 as a potential diagnostic biomarker and therapeutic target for RA." @default.
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- W2016688255 date "2013-04-15" @default.
- W2016688255 modified "2023-09-27" @default.
- W2016688255 title "Deficiency of β-arrestin1 ameliorates collagen-induced arthritis with impaired T<sub>H</sub>17 cell differentiation" @default.
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- W2016688255 doi "https://doi.org/10.1073/pnas.1221608110" @default.
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