T cell-specific BLIMP-1 deficiency exacerbates experimental autoimmune encephalomyelitis in nonobese diabetic mice by increasing Th1 and Th17 cells

doi:10.1016/j.clim.2014.02.006

Chia Nan University of Pharmacy & Science Institutional Repository > 環境永續暨休閒學院 > 休閒保健管理系(所) > 期刊論文 > Item 310902800/28703

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標題:	T cell-specific BLIMP-1 deficiency exacerbates experimental autoimmune encephalomyelitis in nonobese diabetic mice by increasing Th1 and Th17 cells
作者:	Lin, Ming-Hong Yeh, Li-Tzu Chen, Shyi-Jou Chiou, Hsin-Ying C. Chu, Chin-Chen Yen, Linju B. Lin, Kuo-I Chang, Deh-Ming Sytwu, Huey-Kang
貢獻者:	休閒保健管理系
關鍵字:	BLIMP-1 EAE Th1 Th17 Treg IL-10
日期:	2014-04
上傳時間:	2015-05-06 21:25:47 (UTC+8)
出版者:	Academic Press Inc Elsevier Science
摘要:	Recently, we demonstrated that B lymphocyte-induced maturation protein 1 (BLIMP-1) has a role in regulating the differentiation and effector function of Th1 and Th17 tells. As these cells play critical roles in the induction and pathogenesis of experimental autoimmune encephalomyelitis (EAE), we investigated the potential role of T cell BLIMP-1 in modulating MOG(35-55)-induced EAE. We established T cell-specific BLIMP-1 conditional knockout (CKO) NOD mice to dissect the role of BLIMP-1 in EAE using loss-of-function model. Our results indicate that EAE severity is dramatically exacerbated in CKO mice. The numbers of CNS-infiltrating Th1, Th17, IFN-gamma+IL-17A(+), and IL-21(+)IL-17A(+) CD4(+) T cells are remarkably increased in brain and spinal cord of CKO mice. Moreover, the ratio of Tregs/effectors and IL-10 production of Tregs are significantly downregulated in CNS of CKO mice. We conclude that BLIMP-1 suppresses autoimmune encephalomyelitis via downregulating Th1 and Th17 cells and impairing Treg cells. (C) 2014 Elsevier Inc. All rights reserved.
關聯:	Clinical Immunology, v.151 n.2, pp.101-113
顯示於類別:	[休閒保健管理系(所)] 期刊論文

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