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Promoter and Represses Its Expression1
* Department of Cellular Injury, Walter Reed Army Institute of Research, Silver Spring, MD 20910;
Division of Rheumatology, Beth Israel Deaconess Medical Center, Boston, MA 02115; and
Division of Monoclonal Antibodies, Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, MD 20857
The Fc receptor (FcR) 
-chain has been shown to be up-regulated in T cells when the TCR 
-chain is decreased. We demonstrate that Elf-1, but not other Ets family transcription factors, bind to a cluster of GGAA sites located within the 200 bp upstream from the transcription initiation site of the FcR promoter. Forced expression of Elf-1 results in the suppression of FcR expression, whereas silencing its expression with small interfering RNA Elf-1 results in increased FcR expression. Elf-1 represents the first transcription factor identified to be involved in the transcriptional regulation of FcR, and cells that fail to express Elf-1, as is the case with human systemic lupus erythematosus T cells, will express FcR-chain.
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1 This work was supported by National Institutes of Health Grants RO1 AI42269 and RO1 AI49954. The opinions expressed herein are those of the authors and do not reflect those of the Department of Defense.
2 Y.-T.J. and L.S. contributed equally to this study.
3 Address correspondence and reprint requests to Dr. George C. Tsokos, Beth Israel Deaconess Medical Center, 4 Blackfan Circle, HIM-244, Boston, MA 02115. E-mail address: gtsokos{at}bidmc.harvard.edu
4 Abbreviations used in this paper: FcR, Fc receptor; poly(dI-dC), polydeoxyinosinic-deoxycytidylic acid; siRNA, small interfering RNA; SLE, systemic lupus erythematous.
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