Skip Navigation


International Immunology Advance Access originally published online on September 6, 2004
International Immunology 2004 16(10):1355-1364; doi:10.1093/intimm/dxh132
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/10/1355    most recent
dxh132v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (11)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Park, W. S.
Right arrow Articles by Jung, K. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Park, W. S.
Right arrow Articles by Jung, K. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© 2004 The Japanese Society for Immunology

T cell expression of CIITA represses Th1 immunity

Weon Seo Park1, Youngmee Bae1, Doo Hyun Chung3, Yoon-La Choi3,4, Byoung Kwon Kim3, Young Chul Sung5, Eun Young Choi3,4, Seong Hoe Park3,4 and Kyeong Cheon Jung2

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

Correspondence to: S. H. Park; E-mail: pshoe{at}plaza.snu.ac.kr

Correspondence to: K. C. Jung; E-mail: jungkc66{at}snu.ac.kr

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

Transmitting editor: E. Simpson


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 JEMHome page
W. Li, M. H. Sofi, N. Yeh, S. Sehra, B. P. McCarthy, D. R. Patel, R. R. Brutkiewicz, M. H. Kaplan, and C.-H. Chang
Thymic selection pathway regulates the effector function of CD4 T cells
J. Exp. Med., September 3, 2007; 204(9): 2145 - 2157.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.