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ROG Negatively Regulates T-Cell Activation but Is Dispensable for Th-Cell Differentiation

Bok Yun Kang,^1,2, Shi-Chuen Miaw,^1,, and I-Cheng Ho^1,2,3*

Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Brigham and Women's Hospital,¹ Harvard Medical School,³ Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts²

Received 15 September 2004/ Accepted 23 October 2004

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-B activity. ROG-deficient dendritic cells also produce more IL-12p40, another NF-B 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-B. Its mechanism of action and its expression pattern are distinct from those of other transcription factors negatively regulating the activation of T cells.

B.Y.K. and S.-C.M. contributed equally to this work.

Present address: Graduate Institute of Immunology, National Taiwan University, College of Medicine, Taipei 10010, Taiwan.

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