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Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294
Address all correspondence and requests for reprints to: Dr. Etty N. Benveniste, Department of Cell Biology, University of Alabama at Birmingham, 1530 3rd Avenue South, MCLM 395, Birmingham, Alabama 35294-0005. E-mail: tika{at}uab.edu.
Major histocompatibility complex (MHC) class II proteins are important for the initiation of immune responses and are essential for specific recognition of foreign antigens by the immune system. Regulation of class II MHC expression primarily occurs at the transcriptional level. The class II transactivator protein is the master regulator that is essential for both constitutive and interferon-
-inducible class II MHC expression. Estrogen [17ß-estradiol (17ß-E2)] has been shown to have immunomodulatory effects. In this study, we show that 17ß-E2 down-regulates interferon- inducible class II MHC protein levels on brain endothelial cells, as well as other cell types (astrocytes, fibrosacroma cells, macrophages). The inhibitory effects of 17ß-E2 on class II MHC expression are not due to changes in class II transactivator mRNA or protein levels, rather, 17ß-E2 mediates inhibition at the level of class II MHC gene expression. We demonstrate that 17ß-E2 attenuates H3 and H4 histone acetylation and cAMP response element binding protein-binding protein association with the class II MHC promoter, suggesting that 17ß-E2 inhibits class II MHC expression by a novel mechanism involving modification of the histone acetylation status of the class II MHC promoter.
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