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* Institute of Biochemistry,
World Health Organization-Immunology Research and Training Center, Institute of Biochemistry, and
Ludwig Institute for Cancer Research, Lausanne Branch, University of Lausanne, Epalinges, Switzerland;
Institut für Medizinische Mikrobiologie, Marburg, Germany;
¶ Dipartimento di Medicina Interna, Sezione di Immunoallergologia e Malattie dell’Apparato Respiratorio, Universita’ degli Studi di Firenze, Firenze, Italy;
|| Max-Planck-Institut für Immunbiologie, Hans-Spemann Laboratories, Freiburg, Germany; and
# Department of Genetics and Microbiology, University of Geneva Medical School, Geneva, Switzerland
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.
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