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 Blood, 15 November 2005, Vol. 106, No. 10, pp. 3440-3448.
Prepublished online as a Blood First Edition Paper on August 9, 2005; DOI 10.1182/blood-2005-03-0857.

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IMMUNOBIOLOGY

Transcription factor GATA-1 potently represses the expression of the HIV-1 coreceptor CCR5 in human T cells and dendritic cells

Mark S. Sundrud, Scott E. VanCompernolle, Karla A. Eger, Tullia C. Bruno, Arun Subramaniam, Srinivas Mummidi, Sunil K. Ahuja, and Derya Unutmaz

From the Department of Microbiology and Immunology, Vanderbilt University Medical School, Nashville, TN; the Veterans Administration Center for AIDS and HIV Infection, South Texas Veterans Health Care System, San Antonio, TX; the Department of Medicine, University of Texas Health Science Center, San Antonio, TX; and the Department of Internal Medicine, Sanofi Aventis Pharmaceuticals, Bridgewater, NJ.

CC chemokine receptor 5 (CCR5) is the major HIV-1 coreceptor and its expression levels are a critical determinant of HIV-1 infection. However, the molecular mechanisms of CCR5 regulation in primary targets of HIV-1 remain unknown. Despite binding to conserved DNA elements, we show that the transcription factors GATA binding protein 1 (GATA-1) and GATA-3 differentially suppress the expression of CCR5 in stem-cell–derived dendritic cells and primary human T-cell subsets. In addition, GATA-1 expression was also more potent than GATA-3 in suppressing T helper 1 (Th1)–associated genes, interferon-{gamma} (IFN{gamma}), and CXC chemokine receptor-3 (CXCR3). GATA-1, but not GATA-3, potently suppressed CCR5 transcription, thereby rendering human T cells resistant to CCR5-tropic HIV-1 infection. However, GATA-1 could also serve as a surrogate for GATA-3 in its canonic role of programming Th2 gene expression. These findings provide insight into GATA-3–mediated gene regulation during T-cell differentiation. Importantly, decoding the mechanisms of GATA-1–mediated repression of CCR5 may offer an opportunity to develop novel approaches to inhibit CCR5 expression in T cells.


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