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Deciphering the tête-à-tête between the microbiota and the immune system
Neeraj K. Surana, Dennis L. Kasper
Neeraj K. Surana, Dennis L. Kasper
Published July 18, 2014
Citation Information: J Clin Invest. 2014;124(10):4197-4203. https://doi.org/10.1172/JCI72332.
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Deciphering the tête-à-tête between the microbiota and the immune system

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Abstract

The past decade has witnessed an explosion in studies — both clinical and basic science — examining the relationship between the microbiota and human health, and it is now clear that the effects of commensal organisms are much broader than previously believed. Among the microbiota’s major contributions to host physiology is regulation of the development and maintenance of the immune system. There are now a handful of examples of intestinal commensal bacteria with defined immunomodulatory properties, but our mechanistic understanding of how microbes influence the immune system is still in its infancy. Nevertheless, several themes have emerged that provide a framework for appreciating microbe-induced immunoregulation. In this Review, we discuss the current state of knowledge regarding the role of the intestinal microbiota in immunologic development, highlighting mechanistic principles that can guide future work.

Authors

Neeraj K. Surana, Dennis L. Kasper

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Figure 1

Commensal bacteria that modulate the intestinal immune system.

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Commensal bacteria that modulate the intestinal immune system.
SFB induc...
SFB induces Th17 in the intestinal lamina propria via a mechanism that involves host production of serum amyloid A (SAA). B. fragilis has pleiotropic effects: it produces a glycosphingolipid (GSL) that inhibits iNKT cell proliferation in the colonic lamina propria; in contrast, B. fragilis PSA interacts with TLR2 on DCs to induce colonic Tregs. A group of Clostridium species taken en masse and individual species within the order Bacteroidales (Bacteroides caccae, Bacteroides massiliensis, Bacteroides thetaiotaomicron, Bacteroides vulgatus, and Parabacteroides distasonis) have been demonstrated to induce colonic Tregs, presumably via bacterial production of SCFAs.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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