Th17 cells in type 1 diabetes

被引：93

作者：

Shao, Shiying ^{[1
]}

He, Fan ^{[2
]}

Yang, Yan ^{[1
]}

Yuan, Gang ^{[1
]}

Zhang, Muxun ^{[1
]}

Yu, Xuefeng ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Div Endocrinol, Tongji Hosp, Tongji Med Coll, Wuhan 430074, Hubei Provience, Peoples R China

[2] Huazhong Univ Sci & Technol, Div Nephrol, Tongji Hosp, Tongji Med Coll, Wuhan 430074, Hubei Provience, Peoples R China

来源：

CELLULAR IMMUNOLOGY | 2012年 / 280卷 / 01期

基金：

中国国家自然科学基金;

关键词：

Type; 1; diabetes; T helper 17 cell; Autoimmunity; Regulatory T cell; Effector T cell; REGULATORY T-CELLS; IL-21; NOD; DIFFERENTIATION; EXPRESSION; INDUCTION; T(H)17; LEADS; IL-17; INFLAMMATION;

D O I：

10.1016/j.cellimm.2012.11.001

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

T1D is an autoimmune disorder, which involves the CD4(+) as well as CD8(+) T-cell-mediated destruction of beta cells. Recently, another population of T cells (Th17) is found to be involved in T1D pathology. This review will discuss the characteristics of Th17 cells and the mechanism of Th17-mediated T1D development. Th17 cell expansion is unstrained under T1D condition. Certain Treg cells are defective in T1D and lose the control of Th17 expansion. In addition, the altered function of APCs and a subset of monocytes which spontaneously secrete IL-1 beta and IL-6 in T1D determine the abnormal expansion of Th17 as well. The pathogenic Th17 cells can cause the imbalance between Teff and Treg cells. Conversion from Th17 to Th1 phenotype and Th17 stimulated CTL responses may play an accessory role in T1D as well. Due to the effects of Th17 on T1D, therapeutic strategies designed to inhibit these cells are applicable and the positive effects are obvious. Taken together, Th17 may exert essential effects on the development of T1D. Identification of the underlying mechanism may inspire new viewpoints for the therapy of this disease. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：16 / 21

页数：6

共 49 条

[1] Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17 [J].