Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan.
Hum Genet. 2010 Apr;127(4):411-9. doi: 10.1007/s00439-009-0781-z.
Although the exact pathogenesis of subacute sclerosing panencephalitis (SSPE) remains to be determined, our previous data suggested a genetic contribution to the host susceptibility to SSPE. During chronic viral infection, virus-specific cytotoxic T lymphocytes display poor effector functions. Since co-inhibitory molecules are involved in the suppression of T lymphocytes, we investigated whether single nucleotide polymorphisms (SNPs) of genes encoding co-inhibitory molecules contributed to a susceptibility to SSPE. Association studies on a total of 20 SNPs in 8 genes (CTLA4, CD80, CD86, PD1, PDL1, PDL2, BTLA and HVEM) and subsequent haplotype analysis of 4 SNPs in the PD1 genes were performed in Japanese and Filipino SSPE patients and controls. Then, we investigated a functional difference in promoter activity of two haplotypes and compared the expression levels of PD1 between SSPE and controls. The frequency of GCG(C) haplotype of PD1 containing -606G allele was significantly higher in SSPE patients than in controls both in Japanese and in Filipinos. The promoter activity was significantly higher in the construct with -606G allele than in that with -606A allele. The expression levels of PD1 were significantly higher in SSPE patients than in the controls. Our results suggested that the PD1 gene contributed to a genetic susceptibility to SSPE.
虽然亚急性硬化性全脑炎(SSPE)的确切发病机制仍有待确定,但我们之前的数据表明宿主易患 SSPE 与遗传因素有关。在慢性病毒感染期间,病毒特异性细胞毒性 T 淋巴细胞表现出较差的效应功能。由于共抑制分子参与 T 淋巴细胞的抑制,我们研究了编码共抑制分子的基因中的单核苷酸多态性(SNP)是否导致 SSPE 易感性。对来自日本和菲律宾的 SSPE 患者和对照组的 8 个基因(CTLA4、CD80、CD86、PD1、PDL1、PDL2、BTLA 和 HVEM)中的总共 20 个 SNP 进行了关联研究,并对 PD1 基因中的 4 个 SNP 进行了随后的单倍型分析。然后,我们研究了两种单倍型启动子活性的功能差异,并比较了 SSPE 和对照组之间 PD1 的表达水平。在日本和菲律宾的 SSPE 患者中,PD1 基因中含有-606G 等位基因的 GCG(C)单倍型的频率明显高于对照组。含有-606G 等位基因的构建体的启动子活性明显高于含有-606A 等位基因的构建体。PD1 的表达水平在 SSPE 患者中明显高于对照组。我们的结果表明,PD1 基因与 SSPE 的遗传易感性有关。