T cell expression of CIITA represses Th1 immunity
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SCOPUS
- Title
- T cell expression of CIITA represses Th1 immunity
- Authors
- Park, WS; Bae, Y; Chung, DH; Choi, YL; Kim, BK; Sung, YC; Choi, EY; Park, SH; Jung, KC
- Date Issued
- 2004-10
- Publisher
- OXFORD UNIV PRESS
- 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 p56(lck), 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 MOG(35-55), while the proliferation of MOG(35-55)-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; CLASS-II TRANSACTIVATOR; INTERFERON-GAMMA; GENE-EXPRESSION; FAS LIGAND; MICE; TRANSCRIPTION; IL-4; DIFFERENTIATION; LYMPHOCYTES; PROMOTER
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/17693
- DOI
- 10.1093/intimm/dxh132
- ISSN
- 0953-8178
- Article Type
- Article
- Citation
- INTERNATIONAL IMMUNOLOGY, vol. 16, no. 10, page. 1355 - 1364, 2004-10
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