期刊
JOURNAL OF IMMUNOLOGY
卷 186, 期 10, 页码 5638-5647出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1003801
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资金
- National Cancer Institute [1RC1CA146576-01, 2R01CA076340-11A2]
- Department of Defense [W81XWH-10-1-0466]
- Grants-in-Aid for Scientific Research [23390015, 23790067] Funding Source: KAKEN
Earlier, we demonstrated the essential role of Kruppel-like transcription factor, TIEG1, in TGF-beta-induced regulatory T cell (Treg) development. In this article, we demonstrate that IL-6, which promotes Th17 development, abrogated TIEG1 nuclear translocation and inhibited TGF-beta-induced Treg development. Tyrosine kinase Tyk2-mediated phosphorylation of TIEG1 at Tyr179 promoted noncanonical K-27-linked polyubiquitination, which inhibited TIEG1 nuclear translocation. To test the role of TIEG1-regulated Treg/Th17 development in antitumor immunity, we analyzed TRAMP-C2 tumor growth in TIEG1(-/-) mice. The defective Treg development and elevated Th17 response resulted in enhanced immune reactivity in the tumor and inhibition of TRAMP-C2 tumor growth in TIEG1(-/-) mice. Thus, our results uncovered a novel regulatory mechanism that modulates Tregs and may regulate tumor progression. The Journal of Immunology, 2011, 186: 5638-5647.
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