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International Immunology Advance Access published online on September 6, 2004
International Immunology, doi:10.1093/intimm/dxh132
© 2004 by The Japanese Society for Immunology
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Received February 11, 2004
Accepted June 17, 2004

Article

T cell expression of CIITA represses Th1 immunity

Weon Seo Park 1, Youngmee Bae 1, Doo Hyun Chung 2, Yoon-La Choi 3, Byoung Kwon Kim 2, Young Chul Sung 4, Eun Young Choi 3, Seong Hoe Park 3*, and Kyeong Cheon Jung 5

1 Department of Pathology, Kangwon University College of Medicine, Chunchon, Korea
2 Department of Pathology, College of Medicine, Seoul, Korea
3 Department of Pathology, College of Medicine, Seoul, Korea; Research Division for Human Life Science, Seoul National University, Seoul, Korea
4 Department of Life Science, Pohang University of Science and Technology, Pohang, Korea
5 Department of Pathology, Hallym University College of Medicine, Chunchon, Korea

* To whom correspondence should be addressed. E-mail: pshoe{at}plaza.snu.ac.kr.


  Abstract

Despite the fact that major histocompatibility complex class II transactivator (CIITA) has been known to be involved in Th1/Th2 balance in addition to its major role as a master regulator for the expression of MHC class II genes, the exact role of CIITA in Th1/Th2 balance is still controversial. To investigate whether the Th1/Th2 balance could be modulated by T cell specific expression of CIITA, we generated CIITA-transgenic mice, in which the CIITA expression is controlled by the distal promoter of p56lck, resulting in constitutive expression of CIITA predominantly in peripheral T cells. Naive CD4+ T cells from CIITA-transgenic mice exhibited a low level of IFN-{gamma} secretion as well as impaired Th1 polarization in vitro, while IL-4 secretion was enhanced under Th2 condition. In addition, the development of experimental autoimmune encephalomyelitis (EAE), a prototype of Th1-mediated disease, was repressed in CIITA-transgenic mice. Resistance to EAE was correlated with reduced production of IFN-{gamma} in response to MOG35-55, while the proliferation of MOG35-55-specific T cells was not affected in CIITA-transgenic mice. Together, these data demonstrate that overexpression of CIITA in T cells inhibits Th1 differentiation and function, suggesting that the expression of CIITA in T cells might play a role in the regulation of the Th1/Th2 balance during the T cell lineage commitment.

Keywords: experimental autoimmune encephalomyelitis; IFN-{gamma}; MHC class II; transgenic mouse.
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