CD8alpha+ dendritic cells prime TCR-peptide-reactive regulatory CD4+FOXP3- T cells.
CD8alpha+ dendritic cells prime TCR-peptide-reactive regulatory CD4+FOXP3- T cells.
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DOI：
10.1002/eji.200939608
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发表时间：
2010-07
影响因子：
5.4
通讯作者：
Kumar, Vipin
中科院分区：
文献类型：
--
作者：
Smith, Trevor R. F.;Maricic, Igor;Ria, Francesco;Schneider, Susan;Kumar, Vipin
具有免疫调节功能的CD4+ T细胞可以是FOXP3+，也可以是FOXP3−。我们之前已经证明，启动自然发生的tcr肽反应性调节性CD4+FOXP3−T细胞（Treg）特异性控制介导实验性自身免疫性脑脊髓炎（EAE）的Vβ8.2+CD4+ T细胞。然而，这些Treg识别同源抗原决定因子（来自tcrv β8.2链）的机制尚不清楚。在这项研究中，我们发现来自naïve小鼠脾细胞的抗原提呈细胞（APC）能够在缺乏外源抗原的情况下刺激克隆的CD4+ Treg，并且在EAE过程中其刺激能力增强。在APC种群中，DC对Treg的刺激效果最好。CD4+ Treg的刺激依赖于摄入Vβ8.2TCR+ CD4+ T细胞的TCR肽的加工和提呈。此外，树突状细胞与TCR肽脉冲或凋亡的Vβ8.2+ T细胞能够在体内启动Treg并以cd8依赖的方式介导对疾病的保护。这些数据强调了CD8α+ DC启动CD4+ Treg的新机制，并提示了一条可用于启动抗原特异性调节T细胞介导的炎症性疾病的途径。
CD4+ T cells with immune regulatory function can be either FOXP3+ or FOXP3−. We have previously shown that priming of naturally occurring TCR-peptide-reactive regulatory CD4+FOXP3− T cells (Treg) specifically controls Vβ8.2+CD4+ T cells mediating experimental autoimmune encephalomyelitis (EAE). However, the mechanism by which these Treg are primed to recognize their cognate antigenic determinant, which is derived from the TCRVβ8.2-chain, is not known. In this study we show that antigen presenting cells (APC) derived from splenocytes of naïve mice are able to stimulate cloned CD4+ Treg in the absence of exogenous antigen, and their stimulation capacity is augmented during EAE. Among the APC populations DC were the most efficient in stimulating the Treg. Stimulation of CD4+ Treg was dependent upon processing and presentation of TCR peptides from ingested Vβ8.2TCR+ CD4+ T cells. Additionally, dendritic cells pulsed with TCR peptide or apoptotic Vβ8.2+ T cells are able to prime Treg in vivo and mediate protection from disease in a CD8-dependent fashion. These data highlight a novel mechanism for the priming of CD4+ Treg by CD8α+ DC, and suggest a pathway that can be exploited to prime antigen-specific regulation of T cell-mediated inflammatory disease.
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影响因子：
56.9
作者：
HOWELL, MD;WINTERS, ST;BROSTOFF, SW
通讯作者：
BROSTOFF, SW
影响因子：
4.4
作者：
Braciak, TA;Pedersen, B;Kumar, V
通讯作者：
Kumar, V
DOI：
10.1073/pnas.92.21.9510
发表时间：
1995-10-10
影响因子：
11.1
作者：
KUMAR, V;BHARDWAJ, V;SERCARZ, E
通讯作者：
SERCARZ, E
调节性T细胞在类风湿关节炎和抗TNFALPHA治疗中的逆转功能受损。
影响因子：
15.3
作者：
Ehrenstein, MR;Evans, JG;Singh, A;Moore, S;Warnes, G;Isenberg, DA;Mauri, C
通讯作者：
Mauri, C
影响因子：
5.6
作者：
Arrenberg, Philomena;Halder, Ramesh;Kumar, Vipin
通讯作者：
Kumar, Vipin