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首页> 外文期刊>Cellular immunology >Regulatory B cells in infection, inflammation, and autoimmunity
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Regulatory B cells in infection, inflammation, and autoimmunity

机译：感染，炎症和自身免疫中的监管B细胞

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摘要

Regulatory B (Breg) cells are characterized by differential expression of CD5 and CD1d in mouse and CD24 and CD38 in human immune systems. The Breg family also includes LAG-3(+)CD138(hi) plasma cells, CD1d CD5 CD21 CD23 cells, Tim1, PD-L1, PD-L2, CD200- expressing B cells, and CD39(hi)Ki67(+) cells originating from the transitional, marginal zone or germinal centre of the spleen. Breg cells produce IL10 and IL35 and to cause immunosuppression. These cells respond to TLR2, TLR4, and TLR9 agonists, CD40 ligands, IL12p35 and heat shock proteins. Emerging evidence suggests that TLR signalling component Myd88 impacts the modulation of Breg cell responses and the host's susceptibility to infection. Breg cells are found to reduce relapsing-remitting experimental autoimmune encephalomyelitis. However, the Breg-mediated mechanism used to control T cell-mediated immune responses is still unclear. Here, we review the existing literature to find gaps in the current knowledge and to build a pathway to further research.
机译：调节性B（BREG）细胞的特征在于在小鼠和CD24中CD5和CD1D的差异表达，在人免疫系统中的CD38和CD38。 BREG系列还包括LAG-3（+）CD138（HI）等离子体细胞，CD1D CD5 CD21 CD23细胞，TIM1，PD-L1，PD-L2，CD200-表达B细胞和CD39（HI）Ki67（+）细胞源自脾脏的过渡性，边缘区域或生发中心。 BREG细胞产生IL10和IL35并引起免疫抑制。这些细胞响应TLR2，TLR4和TLR9激动剂，CD40配体，IL12P35和热休克蛋白。新兴的证据表明，TLR信令组分MYD88会影响BREG细胞应答的调节和宿主对感染的易感性。发现BREG细胞减少重复依赖性实验性自身免疫脑炎。然而，用于控制T细胞介导的免疫应答的Breg介导的机制仍然不清楚。在这里，我们审查现有文献，以了解当前知识中的差距，并建立进一步研究的途径。

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