CD8+ T activation attenuates CD4+ T proliferation through dendritic cells modification

被引:12
作者
Chen, Dongwei [1 ]
Wang, Ying [1 ]
Wang, Huan [1 ]
Wu, Yiqing [1 ]
Xia, Sheng [2 ]
Zhang, Minghui [1 ]
机构
[1] Tsinghua Univ, Med Ctr, Inst Immunol, Beijing 100084, Peoples R China
[2] Jiangsu Univ, Sch Med, Dept Immunol, Zhenjiang, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
CD8(+) T cell; Dendritic cell; CD4(+) T cell; Immune tolerance; Asthma; ALLERGIC AIRWAY DISEASE; IFN-GAMMA; IN-VIVO; AUTOIMMUNE-DISEASES; STROMAL CELLS; TOLERANCE; RESPONSES; DIFFERENTIATION; INFLAMMATION; MICE;
D O I
10.1016/j.cellimm.2015.05.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Emerging evidence has suggested that CD8(+) T had modulatory function on CD4(+) T mediated autoimmune and inflammatory diseases. However, the underlying mechanisms remain unclear. In this study, we found that CD8(+) T activation inhibited OVA(323-339) antigen specific CD4(+) T cells proliferation in vitro and in vivo. Further investigation demonstrated that this immunosuppression largely depended on the soluble factor from activated CD8(+) T to modify the phenotype and functions of DCs. Moreover, not only the inhibitors for IDO or iNOS, but also IFN-gamma, neutralization markedly reversed this immunosuppression on OVA(323-339) antigen specific CD4(+) T cells proliferation. Interestingly, CD8(+) T cells absence aggravated the pathological damage in lung in OVA-induced asthma model, but alleviated by CD8(+) T transfer and activation. Thus, these findings suggested that activated CD8(+) T population exerted feedback regulation in DCs modification, and then attenuated CD4(+) T mediated immune response. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:138 / 148
页数:11
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