| First Author | Kang BY | Year | 2005 |
| Journal | Mol Cell Biol | Volume | 25 |
| Issue | 2 | Pages | 554-62 |
| PubMed ID | 15632058 | Mgi Jnum | J:94944 |
| Mgi Id | MGI:3522334 | Doi | 10.1128/MCB.25.2.554-562.2005 |
| Citation | Kang BY, et al. (2005) ROG negatively regulates T-cell activation but is dispensable for Th-cell differentiation. Mol Cell Biol 25(2):554-62 |
| abstractText | ROG, a transcriptional repressor, is a direct target gene of NF-AT and a putative negative regulator of T-cell activation. In addition, overexpression of ROG suppresses the activity of GATA-3, implying a role of ROG in the differentiation and function of Th cells. Despite these observations, the function of ROG has yet to be confirmed by loss-of-function approaches. Here we report that ROG-deficient T cells are hypersensitive to anti-CD3 stimulation and produce more interleukin-2 (IL-2) due to enhanced NF-kappaB activity. ROG-deficient dendritic cells also produce more IL-12p40, another NF-kappaB target gene. However, ROG-deficient Th cells are capable of differentiating into Th1 and Th2 cells, and ROG-deficient mice have no defect in mounting appropriate Th immune responses in vivo. Thus, ROG is dispensable for the differentiation and function of Th cells but serves as a mediator of NF-AT-initiated suppression of NF-kappaB. Its mechanism of action and its expression pattern are distinct from those of other transcription factors negatively regulating the activation of T cells. |
