Journal
IMMUNITY
Volume 40, Issue 4, Pages 569-581Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2014.02.012
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Funding
- NIH [P01AI056299, P01AI039671, P01AI073748, R01NS045937, 5T32HL007633, K01DK090105, AI075285, AI09390]
- National Multiple Sclerosis Society [RG4111A1, RG2751]
- Swiss Multiple Sclerosis Society
- Arthritis National Research Foundation
- AGAUR-Government of Catalonia
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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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