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B-1细胞及其与小鼠肠道微生物群的反应性。

B-1 cells and their reactivity with the murine intestinal microflora.

作者信息

Kroese F G, de Waard R, Bos N A

机构信息

Department of Histology and Cell Biology, University of Groningen, Netherlands.

出版信息

Semin Immunol. 1996 Feb;8(1):11-8. doi: 10.1006/smim.1996.0003.

DOI:10.1006/smim.1996.0003
PMID:8850294
Abstract

IgA secreting cells located in the lamina propria of the gut are a prominent feature of the mucosal immune system, which serves to protect the body from the continuous threat to infection by intestinal bacteria. In this review we summarize briefly the evidence that these IgA secreting cells have a dual origin and are derived either from conventional B cells or from B-1 cells. Furthermore, we show both at polyclonal and monoclonal levels that the major antigenic target of B-1 cell derived IgA are normal intestinal bacteria. Coating of intestinal bacteria with IgA is thought to result in immune exclusion, as shown for pathogenic bacteria. However, the bacterial microflora of the gut is an extremely stable ecosystem, despite the fact that the majority of intestinal bacteria are coated with IgA. We speculate here that these apparent contradictory functions of the humoral immune system, i.e. removal of bacteria and maintaining the normal gut flora might be exerted by IgA antibodies produced by the two B-cell lineages. The fixed and biased repertoire of B-1 cells might play a role in maintaining the normal intestinal flora. When pathogenic bacteria penetrate into the gut, conventional B cells may be induced in the Peyer's patches to produce high affinity, narrowly tuned IgA antibodies, leading to immune exclusion.

摘要

位于肠道固有层的分泌IgA的细胞是黏膜免疫系统的一个显著特征,该系统旨在保护身体免受肠道细菌持续感染威胁。在本综述中,我们简要总结了这些分泌IgA的细胞具有双重起源且来源于传统B细胞或B-1细胞的证据。此外,我们在多克隆和单克隆水平均表明,B-1细胞衍生的IgA的主要抗原靶点是正常肠道细菌。正如针对病原菌所显示的那样,IgA包被肠道细菌被认为会导致免疫排斥。然而,尽管大多数肠道细菌都被IgA包被,但肠道细菌微生物群是一个极其稳定的生态系统。我们在此推测,体液免疫系统的这些明显相互矛盾的功能,即清除细菌和维持正常肠道菌群,可能由两个B细胞谱系产生的IgA抗体发挥作用。B-1细胞固定且有偏向性的抗原受体库可能在维持正常肠道菌群中发挥作用。当病原菌侵入肠道时,派尔集合淋巴结中的传统B细胞可能会被诱导产生高亲和力、特异性强的IgA抗体,从而导致免疫排斥。

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