Kang, Bok YunBok YunKangSHI-CHUEN MIAWHo, I-ChengI-ChengHo2019-08-062019-08-062005-010270-7306https://www.scopus.com/inward/record.uri?eid=2-s2.0-11844291981&doi=10.1128%2fMCB.25.2.554-562.2005&partnerID=40&md5=a1b532c394c34970296110fba4232f08https://scholars.lib.ntu.edu.tw/handle/123456789/416259ROG, 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.enjournal article10.1128/MCB.25.2.554-562.2005156320582-s2.0-11844291981WOS:000226287800004https://api.elsevier.com/content/abstract/scopus_id/11844291981