在进行性内脏利什曼病期间，调节性IgDhi B细胞通过IL-10和PD-L1抑制T细胞功能。
Regulatory IgDhi B Cells Suppress T Cell Function via IL-10 and PD-L1 during Progressive Visceral Leishmaniasis.
作者信息
Schaut Robert G, Lamb Ian M, Toepp Angela J, Scott Benjamin, Mendes-Aguiar Carolina O, Coutinho Jose F V, Jeronimo Selma M B, Wilson Mary E, Harty John T, Waldschmidt Thomas J, Petersen Christine A
机构信息
Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA 52242;
Department of Biochemistry, Health Graduate Program, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal 1655, 59072-970, Brazil; Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fiocruz, Rio de Janeiro 4365, 21045-900, Brazil;
出版信息
J Immunol. 2016 May 15;196(10):4100-9. doi: 10.4049/jimmunol.1502678. Epub 2016 Apr 13.
During visceral leishmaniasis (VL), Th1-based inflammation is induced to control intracellular parasites. Inflammation-based pathology was shown to be dampened by IL-10 and eventual programmed death 1-mediated T cell exhaustion. Cell type(s) responsible for the initiation of T cell-produced IL-10 during VL are unknown. CD19(+), CD5(-), CD1d(-), IgD(hi) regulatory B cells from healthy controls produced IL-10 in the absence of infection or stimulation, in contrast to IgD(lo/neg) B cells. IgD(hi) B cells may have a de novo versus induced regulatory program. The population of IgD(hi) B cells increased 3-fold as VL progressed. B cells from VL dogs were necessary and sufficient to suppress Th1 cell effector function. IgD(hi) B cells induced IL-10 production by T cells and IgD(lo) B cells. Blockage of B cell-specific PD-L1 restored Th1 responses. IgD(hi) regulatory B cells represent a novel regulatory B cell that may precipitate T cell exhaustion during VL.
在内脏利什曼病（VL）期间，会诱导基于Th1的炎症反应来控制细胞内寄生虫。研究表明，基于炎症的病理反应会被IL-10以及最终程序性死亡1介导的T细胞耗竭所抑制。VL期间负责启动T细胞产生IL-10的细胞类型尚不清楚。与IgD（低/阴性）B细胞相比，来自健康对照的CD19（+）、CD5（-）、CD1d（-）、IgD（高）调节性B细胞在无感染或刺激的情况下产生IL-10。IgD（高）B细胞可能具有全新的与诱导性调节程序。随着VL的进展，IgD（高）B细胞群体增加了3倍。来自VL犬的B细胞对于抑制Th1细胞效应功能是必要且充分的。IgD（高）B细胞诱导T细胞和IgD（低）B细胞产生IL-10。阻断B细胞特异性PD-L1可恢复Th1反应。IgD（高）调节性B细胞代表一种新型调节性B细胞，可能在VL期间促使T细胞耗竭。
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