Juang Yuang-Taung, Sumibcay Laarni, Tolnay Mate, Wang Ying, Kyttaris Vasileios C, Tsokos George C
Department of Cellular Injury, Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA.
J Immunol. 2007 Oct 1;179(7):4884-9. doi: 10.4049/jimmunol.179.7.4884.
The Fc receptor (FcR) gamma-chain has been shown to be up-regulated in T cells when the TCR zeta-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 FcRgamma promoter. Forced expression of Elf-1 results in the suppression of FcRgamma expression, whereas silencing its expression with small interfering RNA Elf-1 results in increased FcRgamma expression. Elf-1 represents the first transcription factor identified to be involved in the transcriptional regulation of FcRgamma, and cells that fail to express Elf-1, as is the case with human systemic lupus erythematosus T cells, will express FcRgamma-chain.
当T细胞受体ζ链减少时，Fc受体（FcR）γ链在T细胞中被上调。我们证明，Elf-1而非其他Ets家族转录因子，可与位于FcRγ启动子转录起始位点上游200 bp内的GGAA位点簇结合。Elf-1的强制表达导致FcRγ表达的抑制，而用小干扰RNA沉默其表达则导致FcRγ表达增加。Elf-1是首个被鉴定参与FcRγ转录调控的转录因子，而像人类系统性红斑狼疮T细胞那样未能表达Elf-1的细胞，将会表达FcRγ链。
