并非总是反派：B细胞作为自身免疫性病理的调节因子。

Not always the bad guys: B cells as regulators of autoimmune pathology.

作者信息

Fillatreau Simon, Gray David, Anderton Stephen M

机构信息

Simon Fillatreau is at the Immune regulation group, Deutsches Rheuma-ForschungsZentrum, Charitéplatz 1, 10117 Berlin, Germany.

出版信息

Nat Rev Immunol. 2008 May;8(5):391-7. doi: 10.1038/nri2315.

DOI:10.1038/nri2315

PMID:18437156

Abstract

When B cells react aggressively against self, the potential for pathology is extreme. It is therefore not surprising that B-cell depletion is seen as an attractive therapy in autoimmune diseases. However, B cells can also be essential for restraining unwanted autoaggressive T-cell responses. Recent advances have pointed to interleukin-10 (IL-10) production as a key component in B-cell-mediated immune regulation. In this Opinion article, we develop a hypothesis that triggering of Toll-like receptors controls the propensity of B cells for IL-10 production and immune suppression. According to this model, B cells can translate exposure to certain microbial infections into protection from chronic inflammatory diseases.

摘要

当B细胞对自身产生强烈反应时，引发病变的可能性极大。因此，B细胞耗竭被视为自身免疫性疾病的一种有吸引力的治疗方法也就不足为奇了。然而，B细胞对于抑制不必要的自身攻击性T细胞反应也可能至关重要。最近的研究进展表明，白细胞介素-10（IL-10）的产生是B细胞介导的免疫调节的关键组成部分。在这篇观点文章中，我们提出了一个假说，即Toll样受体的触发控制着B细胞产生IL-10和免疫抑制的倾向。根据这个模型，B细胞可以将接触某些微生物感染转化为对慢性炎症性疾病的保护。