Commensal microbes drive intestinal inflammation by IL-17–producing CD4~+ T cells through ICOSL and OX40L costimulation in the absence of B7-1 and B7-2

Lijun Xina; Tony T. Jiang; Vandana ChaturvediJeremy M. KinderJames M. ErteltJared H. RoweKris A. SteinbrecherSing Sing Way

首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Commensal microbes drive intestinal inflammation by IL-17–producing CD4~+ T cells through ICOSL and OX40L costimulation in the absence of B7-1 and B7-2

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Commensal microbes drive intestinal inflammation by IL-17–producing CD4~+ T cells through ICOSL and OX40L costimulation in the absence of B7-1 and B7-2

机译：Commensal microbes drive intestinal inflammation by IL-17–producing CD4~+ T cells through ICOSL and OX40L costimulation in the absence of B7-1 and B7-2

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The costimulatory B7-1 (CD80)/B7-2 (CD86) molecules, along with T-cell receptor stimulation, together facilitate T-cell activation. This explains why in vivo B7 costimulation neutralization efficiently silences a variety of human autoimmune disorders. Paradoxically, however, B7 blockade also potently moderates accumulation of immune- suppressive regulatory T cells (Tregs) essential for protection against multiorgan systemic autoimmunity. Here we show that B7 deprivation in mice overrides the necessity for Tregs in averting systemic autoimmunity and inflammation in extraintestinal tissues, whereas peripherally induced Tregs retained in the absence of B7 selectively mitigate intestinal inflammation caused by Th17 effector CD4~+ T cells. The need for additional immune suppression in the intestine reflects commensal microbe-driven T-cell activation through the accessory costimulation molecules ICOSL and OX40L. Eradication of commensal enteric bacteria mitigates intestinal inflammation and IL-17 production triggered by Treg depletion in B7-deficient mice, whereas re-establishing intestinal colonization with Candida albicans primes expansion of Th17 cells with commensal specificity. Thus, neutralizing B7 costimulation uncovers an essential role for Tregs in selectively averting intestinal inflammation by Th17 CD4~+ T cells with commensal microbe specificity.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2014年第29期|10672-10677|共6页
作者
Lijun Xina; Tony T. Jiang; Vandana ChaturvediJeremy M. KinderJames M. ErteltJared H. RoweKris A. SteinbrecherSing Sing Way;
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作者单位

Divisions of Infectious Diseases, Cincinnati Children's Hospital, Cinncinnati, OH 45229;

Divisions of Gastroenterology, Cincinnati Children's Hospital, Cinncinnati, OH 45229;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
microbes; inflammation; absence;

Commensal microbes drive intestinal inflammation by IL-17–producing CD4~+ T cells through ICOSL and OX40L costimulation in the absence of B7-1 and B7-2

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