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在Foxp3⁺调节性T细胞诱导之前,产生白细胞介素-10的B细胞在幽门螺杆菌感染后会扩增。

Prior to Foxp3⁺ regulatory T-cell induction, interleukin-10-producing B cells expand after Helicobacter pylori infection.

作者信息

Wei Lumin, Wang Jingtong, Liu Yulan

机构信息

Department of Gastroenterology, Peking University People's Hospital, Beijing, China.

出版信息

Pathog Dis. 2014 Oct;72(1):45-54. doi: 10.1111/2049-632X.12182. Epub 2014 May 21.

Abstract

Regulatory T (Treg) cells play a critical role in Helicobacter pylori immune evasion and persistent infection. In addition to Treg cells, it is still unknown whether a newly defined B-cell subset, interleukin (IL)-10-producing B cells, is involved. Using a mouse model of H. pylori infection, we investigated the dynamic changes of IL-10-producing B cells and Foxp3(+) Treg cells in gastrointestinal mucosa, spleen and mesenteric lymph nodes following H. pylori infection. We observed that in addition to Foxp3(+) Treg cells, IL-10-producing B cells could also be induced after H. pylori infection and they expanded earlier than Foxp3(+) Treg cells did. Moreover, the regulatory immune responses induced by H. pylori were not limited to gastric mucosa. Our findings may provide new clues for further research on H. pylori immune evasion and diseases associated with H. pylori infection.

摘要

调节性T(Treg)细胞在幽门螺杆菌免疫逃逸和持续感染中起关键作用。除了Treg细胞外,一种新定义的B细胞亚群,即产生白细胞介素(IL)-10的B细胞是否参与其中仍不清楚。利用幽门螺杆菌感染的小鼠模型,我们研究了幽门螺杆菌感染后胃肠道黏膜、脾脏和肠系膜淋巴结中产生IL-10的B细胞和Foxp3(+)Treg细胞的动态变化。我们观察到,除了Foxp3(+)Treg细胞外,幽门螺杆菌感染后也可诱导产生IL-10的B细胞,且它们比Foxp3(+)Treg细胞更早扩增。此外,幽门螺杆菌诱导的调节性免疫反应并不局限于胃黏膜。我们的发现可能为进一步研究幽门螺杆菌免疫逃逸及与幽门螺杆菌感染相关疾病提供新线索。

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