期刊
JOURNAL OF IMMUNOLOGY
卷 172, 期 1, 页码 170-177出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.1.170
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI045653] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI 45653-01] Funding Source: Medline
The NF-AT family is a group of potent transcription factors that are essential for T cell activation in vitro. However, NF-ATc2-deficient Th cells display hyperproliferation in response to stimulation, suggesting that NF-ATc2 functions as a negative regulator of Th cell activation/proliferation. In this study we show that the transcriptional repressor of GATA (ROG) is a direct target gene of NF-ATc2 and that NF-ATc2-deficient Th cells are unable to fully up-regulate ROG upon stimulation. Restoration of ROG expression in vivo partly corrects the hyperproliferation of NF-ATc2-deficient Th cells by attenuating TCR signals. Our data, therefore, depict a ROG-mediated negative feedback mechanism of T cell activation.
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