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Transcriptional regulation of CD4+ T cell differentiation in experimentally-induced arthritis and rheumatoid arthritis.

Transcriptional regulation of CD4+ T cell differentiation in experimentally-induced arthritis and rheumatoid arthritis.
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Kondo Y, Yokosawa M, Kaneko S, Furuyama K, Segawa S, Tsuboi H, Matsumoto I, Sumida T,


Kondo Y, Yokosawa M, Kaneko S, Furuyama K, Segawa S, Tsuboi H, Matsumoto I, Sumida T, (click to view)

Kondo Y, Yokosawa M, Kaneko S, Furuyama K, Segawa S, Tsuboi H, Matsumoto I, Sumida T,

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Arthritis & rheumatology (Hoboken, N.J.) 2017 12 15() doi 10.1002/art.40398
Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by infiltration of the joint synovium by activated inflammatory cells. CD4+ T cells form a large proportion of the inflammatory cells invading the synovial tissue, and are involved in the RA pathological process. In general, CD4+ T cells differentiate into various T helper (Th) cell subsets and acquire the functional characterization to respond to specific pathogens, and also mediated some autoimmune disorders such as RA. Because the differentiation of Th cell subsets is determined by the expression of specific transcription factors in response to cytokine environment, these transcription factors is considered to have a role in pathology of RA. T regulatory (Treg) cells control an excess of T cell mediated immune response, and the transcription factor Foxp3 is critical for the differentiation and the function of Treg cells, therefore the dysfunction of Treg cells results in the development of systemic autoimmunity. In this review, we summarize how the expression of transcription factors modulates the Th cell immune responses and the development of autoimmune diseases especially in RA. By understanding the role of transcription factors in the pathogenesis of autoimmunity, we may obtain novel therapeutic strategy to control the differentiation and the function in both Th cells and Treg cells. This article is protected by copyright. All rights reserved.

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