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Helicobacter species are potent drivers of colonic T cell responses in homeostasis and inflammation.

Authors :
Chai, Jiani N.
Yangqing Peng
Rengarajan, Sunaina
Solomon, Benjamin D.
Ai, Teresa L.
Zeli Shen
Perry, Justin S. A.
Knoop, Kathryn A.
Takeshi Tanoue
Seiko Narushima
Kenya Honda
Elson, Charles O.
Newberry, Rodney D.
Stappenbeck, Thaddeus S.
Kau, Andrew L.
Peterson, Daniel A.
Fox, James G.
Chyi-Song Hsieh
Source :
Science Immunology; 2017, Vol. 2 Issue 13, p1-12, 12p, 7 Graphs
Publication Year :
2017

Abstract

Specific gut commensal bacteria improve host health by eliciting mutualistic regulatory T (T<subscript>reg</subscript>) cell responses. However, the bacteria that induce effector T (T<subscript>eff</subscript>) cells during inflammation are unclear. We addressed this by analyzing bacterial-reactive T cell receptor (TCR) transgenic cells and TCR repertoires in a murine colitis model. Unexpectedly, we found that mucosal-associated Helicobacter species triggered both T<subscript>reg</subscript> cell responses during homeostasis and T<subscript>eff</subscript> cell responses during colitis, as suggested by an increased overlap between the T<subscript>eff</subscript>/T<subscript>reg</subscript> TCR repertoires with colitis. Four of six T<subscript>reg</subscript> TCRs tested recognized mucosal-associated Helicobacter species in vitro and in vivo. By contrast, the marked expansion of luminal Bacteroides species seen during colitis did not trigger a commensurate T<subscript>eff</subscript> cell response. Unlike other T<subscript>reg</subscript> cell–inducing bacteria, Helicobacter species are known pathobionts and cause disease in immunodeficient mice. Thus, our study suggests a model in which mucosal bacteria elicit context-dependent T<subscript>reg</subscript> or T<subscript>eff</subscript> cell responses to facilitate intestinal tolerance or inflammation. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
24709468
Volume :
2
Issue :
13
Database :
Complementary Index
Journal :
Science Immunology
Publication Type :
Academic Journal
Accession number :
164971049
Full Text :
https://doi.org/10.1126/sciimmunol.aal5068