Dichotomous regulation of group 3 innate lymphoid cells by nongastric Helicobacter species

Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identifi...

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Bibliographic Details
Main Authors: Shen, Zeli (Author), Fox, James G. (Author)
Other Authors: Massachusetts Institute of Technology. Division of Comparative Medicine (Contributor), Massachusetts Institute of Technology. Department of Biological Engineering (Contributor)
Format: Article
Language:English
Published: Proceedings of the National Academy of Sciences, 2020-04-22T12:49:17Z.
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Online Access:Get fulltext
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100 1 0 |a Shen, Zeli  |e author 
100 1 0 |a Massachusetts Institute of Technology. Division of Comparative Medicine  |e contributor 
100 1 0 |a Massachusetts Institute of Technology. Department of Biological Engineering  |e contributor 
700 1 0 |a Fox, James G.  |e author 
245 0 0 |a Dichotomous regulation of group 3 innate lymphoid cells by nongastric Helicobacter species 
260 |b Proceedings of the National Academy of Sciences,   |c 2020-04-22T12:49:17Z. 
856 |z Get fulltext  |u https://hdl.handle.net/1721.1/124784 
520 |a Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identified opposing effects on ILCs by two Helicobacter species, Helicobacter apodemus and Helicobacter typhlonius, isolated from immunocompromised mice. We demonstrated that the introduction of both Helicobacter species activated ILCs and induced gut inflammation; however, these Helicobacter species negatively regulated RORγt+ group 3 ILCs (ILC3s), especially T-bet+ ILC3s, and diminished their proliferative capacity. Thus, these findings underscore a previously unknown dichotomous regulation of ILC3s by Helicobacter species, and may serve as a model for further investigations to elucidate the host-microbe interactions that critically sustain the maintenance of intestinal ILC3s. 
520 |a National Institutes of Health (U.S.) ( Instrumentation Grant 1S10 OD021676-01) 
546 |a en 
690 |a Multidisciplinary 
655 7 |a Article 
773 |t 10.1073/pnas.1908128116 
773 |t Proceedings of the National Academy of Sciences of the United States of America