Immunity
Volume 40, Issue 4, 17 April 2014, Pages 569-581
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Article
Treg Cells Expressing the Coinhibitory Molecule TIGIT Selectively Inhibit Proinflammatory Th1 and Th17 Cell Responses

https://doi.org/10.1016/j.immuni.2014.02.012Get rights and content
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Highlights

  • TIGIT defines a distinct Foxp3+ Treg cell subset

  • TIGIT induces transcription and secretion of the effector molecule Fgl2 in Treg cells

  • TIGIT+ Treg cells suppress proinflammatory Th1 and Th17 not Th2 cell responses

  • Selective suppression by TIGIT+ Treg cells is Fgl2 dependent

Summary

Foxp3+ T regulatory (Treg) cells regulate immune responses and maintain self-tolerance. Recent work shows that Treg cells are comprised of many subpopulations with specialized regulatory functions. Here we identified Foxp3+ T cells expressing the coinhibitory molecule TIGIT as a distinct Treg cell subset that specifically suppresses proinflammatory T helper 1 (Th1) and Th17 cell, but not Th2 cell responses. Transcriptional profiling characterized TIGIT+ Treg cells as an activated Treg cell subset with high expression of Treg signature genes. Ligation of TIGIT on Treg cells induced expression of the effector molecule fibrinogen-like protein 2 (Fgl2), which promoted Treg-cell-mediated suppression of T effector cell proliferation. In addition, Fgl2 was necessary to prevent suppression of Th2 cytokine production in a model of allergic airway inflammation. TIGIT expression therefore identifies a Treg cell subset that demonstrates selectivity for suppression of Th1 and Th17 cell but not Th2 cell responses.

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