Treg cells expressing the coinhibitory molecule TIGIT selectively inhibit proinflammatory Th1 and Th17 cell responses

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 ce...

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Veröffentlicht in:Immunity (Cambridge, Mass.) Jg. 40; H. 4; S. 569
Hauptverfasser: Joller, Nicole, Lozano, Ester, Burkett, Patrick R, Patel, Bonny, Xiao, Sheng, Zhu, Chen, Xia, Junrong, Tan, Tze G, Sefik, Esen, Yajnik, Vijay, Sharpe, Arlene H, Quintana, Francisco J, Mathis, Diane, Benoist, Christophe, Hafler, David A, Kuchroo, Vijay K
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 17.04.2014
Schlagworte:
Animals
Cell Proliferation
Cells, Cultured
Cytokines - metabolism
Eosinophils - immunology
Fibrinogen - genetics
Fibrinogen - immunology
Fibrinogen - metabolism
Forkhead Transcription Factors - metabolism
Gene Expression Profiling
Gene Expression Regulation
Immunosuppression Therapy
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Receptors, Immunologic - genetics
Receptors, Immunologic - immunology
Receptors, Immunologic - metabolism
Respiratory Hypersensitivity - immunology
T-Lymphocyte Subsets - immunology
T-Lymphocytes, Regulatory - immunology
Th1-Th2 Balance
ISSN:1097-4180, 1097-4180
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Zusammenfassung: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.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1097-4180
1097-4180
DOI:10.1016/j.immuni.2014.02.012