國家衛生研究院 NHRI:Item 3990099045/14210
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    题名: Blimp-1 moulds the epigenetic architecture of IL-21-mediated autoimmune diseases through an autoregulatory circuit
    作者: Liu, YW;Fu, SH;Chien, MW;Hsu, CY;Lin, MH;Dong, JL;Lu, RJ;Lee, YJ;Chen, PY;Wang, CH;Sytwu, HK
    贡献者: National Institute of Infectious Diseases and Vaccinology
    摘要: PRDM1 encodes B lymphocyte-induced maturation protein 1 (BLIMP1), also known as a master regulator of T-cell homeostasis. We observed a negative relationship between Blimp-1 and IL-21 based on our previous data that Blimp-1 overexpression in T cells suppresses autoimmune diabetes while Blimp-1 deficient T cells contribute to colitis in NOD mice. Reanalysis of published datasets also reveals an inverse correlation between PRDM1 and IL21 in Crohn's disease. Here, we illustrate that Blimp-1 represses IL-21 by reducing chromatin accessibility and evicting an IL-21 activator c-Maf from the Il21 promoter. Moreover, IL-21-accelerated autoimmune diabetogenesis in small ubiquitin-like modifier-defective c-Maf transgenic mice can be overridden by Blimp-1 overexpression-mediated reduction in permissive chromatin structures at Il21 promoter. An autoregulatory feedback loop to harness IL-21 expression is unveiled by the evidence that addition of IL-21 induces time-dependent Blimp-1 expression and subsequently enriches its binding to the Il21 promoter to suppress IL-21 overproduction. Furthermore, intervention of this feedback loop by IL-21 blockade, IL-21R.Fc administration or IL-21 receptor deletion, attenuates Blimp-1 deficiency-mediated colitis and reinforces the circuit between Blimp-1 and IL-21 in the regulation of autoimmunity. We highlight the translation of Blimp-1-based epigenetic and transcriptomic profiles applicable to a personalized medicine approach in autoimmune diseases.
    日期: 2022-05-03
    關聯: JCI Insight. 2022 May 3;Article number e151614.
    Link to: http://dx.doi.org/10.1172/jci.insight.151614
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2379-3708&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000809964000001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85131771284
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