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Journal Article

Deregulated MHC Class II Transactivator Expression Leads to a Strong Th2 Bias in CD4 T Lymphocytes

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Steimle,  Viktor
Spemann Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Otten, L. A., Tacchini-Cottier, F., Lohoff, M., Annunziato, F., Cosmi, L., Scarpellino, L., et al. (2003). Deregulated MHC Class II Transactivator Expression Leads to a Strong Th2 Bias in CD4 T Lymphocytes. Journal of Immunology, 170(3), 1150-1157.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-9576-4
Abstract
The MHC class II (MHC-II) transactivator (CIITA) is the master transcriptional regulator of genes involved in MHC-II- restricted Ag presentation. Fine tuning of CIITA gene expression determines the cell type-specific expression of MHC-II genes. This regulation is achieved by the selective usage of multiple CIITA promoters. It has recently been suggested that CIITA also contributes to Th cell differentiation by suppressing IL-4 expression in Th1 cells. In this study, we show that endogenous CIITA is expressed at low levels in activated mouse T cells. Importantly CIITA is not regulated differentially in murine and human Th1 and Th2 cells. Ectopic expression of a CIITA transgene in multiple mouse cell types including T cells, does not interfere with normal development of CD4 T cells. However, upon TCR activation the CIITA transgenic CD4 T cells preferentially differentiate into IL-4-secreting Th2-type cells. These results imply that CIITA is not a direct Th1-specific repressor of the IL-4 gene and that tight control over the expression of CIITA and MHC-II is required to maintain the normal balance between Th1 and Th2 responses.