Kurella S, Yaciuk J C, Dozmorov I, Frank M B, Centola M, Farris A D
Arthritis and Immunology Program, Oklahoma Medical Research Foundation, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Genes Immun. 2005 Oct;6(7):596-608. doi: 10.1038/sj.gene.6364245.
Gene expression changes in CD4 + Vbeta8+ T cells energized by in vivo exposure to staphylococcal enterotoxin B (SEB) bacterial superantigen compared to CD4 + Vbeta8+ non-energic T cells were assessed using DNA microarrays containing 5184 murine complementary DNAs. Anergy in splenic T cells of SEB-immunized BALB/c mice was verified by dramatically reduced proliferative capacity and an 8 x overexpression of GRAIL mRNA in CD4 + Vbeta8+ T cells taken from mice 7 days after injection. At an Associative t-test threshold of P<0.0005, 96 genes were overexpressed or detected only in anergic T cells, while 256 genes were suppressed or not detected in anergic T cells. Six of eight differential expressions tested using real-time quantitative PCR were validated. Message for B-Raf was detected only in non-anergic cells, while expression of the TCR signaling modulator Slap (Src-like adapter protein) and the TCR zeta-chain specific phosphatase Ptpn3 was enhanced. Modulation of multiple genes suggests downregulation of Wnt/beta-catenin signaling and enhanced Notch signaling in the anergic cells. Consistent with previous reports in a non-superantigen in vivo anergy model, mRNA for CD18 and the transcription factor Satb1 (special AT-rich-binding protein 1) was increased in SEB-energized T cells. This is the first report of global transcriptional changes in CD4+ T cells made anergic by superantigen exposure.
与CD4 + Vbeta8 + 非失能T细胞相比,利用包含5184个小鼠互补DNA的DNA微阵列评估体内暴露于葡萄球菌肠毒素B(SEB)细菌超抗原后CD4 + Vbeta8 + T细胞中的基因表达变化。通过显著降低的增殖能力以及注射后7天从小鼠体内获取的CD4 + Vbeta8 + T细胞中GRAIL mRNA的8倍过表达,验证了SEB免疫的BALB / c小鼠脾T细胞中的失能状态。在P<0.0005的关联t检验阈值下,96个基因仅在失能T细胞中过表达或被检测到,而256个基因在失能T细胞中被抑制或未被检测到。使用实时定量PCR测试的八个差异表达中有六个得到了验证。B-Raf的信息仅在非失能细胞中被检测到,而TCR信号调节剂Slap(Src样衔接蛋白)和TCR ζ链特异性磷酸酶Ptpn3的表达增强。多个基因的调节表明失能细胞中Wnt / β-连环蛋白信号下调,Notch信号增强。与先前在非超抗原体内失能模型中的报道一致,CD18的mRNA和转录因子Satb1(富含特殊AT序列结合蛋白1)在SEB失能的T细胞中增加。这是关于超抗原暴露导致CD4 + T细胞失能的全球转录变化的首次报道。