Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
J Autoimmun. 2012 May;38(2-3):J216-22. doi: 10.1016/j.jaut.2011.11.008. Epub 2012 Feb 3.
Lupus is less common in men than women, and the reason is incompletely understood. Current evidence indicates that lupus flares when genetically predisposed individuals encounter environmental agents that trigger the disease, and that the environmental contribution is mediated at least in part by T cell DNA demethylation. We hypothesized that lupus disease activity is directly related to total genetic risk and inversely related to T cell DNA methylation levels in each patient. Since women are predisposed to lupus in part because of their second X chromosome, we also hypothesized that men would require a greater genetic risk, a greater degree of autosomal T cell DNA demethylation, or both, to achieve a lupus flare equal in severity to women. Genetic risk was determined by genotyping men and women with lupus across 32 confirmed lupus susceptibility loci. The methylation status of two autosomal genes known to demethylate in T cells in proportion to disease activity, KIR2DL4 (KIR) and PRF1, was measured by bisulfite sequencing. Lupus disease activity was determined by the SLEDAI. Interactions between genetic score, T cell DNA demethylation, and the SLEDAI score were compared between the men and women by regression analysis. Combining the degree of DNA demethylation with the genetic risk score for each patient demonstrated that the (genetic risk)/(DNA methylation) ratio increased directly with disease activity in both men and women with lupus. Importantly, men required a greater (genetic risk)/(DNA methylation) ratio to achieve a SLEDAI score equivalent to women (P = 0.010 for KIR and P = 0.0054 for PRF1). This difference was not explained by a difference in the genetic risk or T cell DNA demethylation alone, suggesting a genetic-epigenetic interaction. These results suggest that genetic risk and T cell DNA demethylation interact in lupus patients to influence the severity of lupus flares, and that men require a higher genetic risk and/or greater degree of T cell DNA demethylation to achieve a lupus flare equal in severity to women.
狼疮在男性中比女性少见,其原因尚不完全清楚。目前的证据表明,当具有遗传易感性的个体接触到引发疾病的环境因素时,狼疮就会发作,而环境因素的作用至少部分是通过 T 细胞 DNA 去甲基化介导的。我们假设狼疮的疾病活动与总遗传风险直接相关,与每位患者的 T 细胞 DNA 甲基化水平呈反比。由于女性易患狼疮部分是因为她们的第二条 X 染色体,我们还假设男性需要更大的遗传风险、更大程度的常染色体 T 细胞 DNA 去甲基化,或者两者兼而有之,才能达到与女性同等严重程度的狼疮发作。通过对患有狼疮的男性和女性在 32 个已确认的狼疮易感性基因座上进行基因分型,确定了遗传风险。通过亚硫酸氢盐测序测量了两个常染色体基因的甲基化状态,这两个基因在 T 细胞中与疾病活动成比例去甲基化,即 KIR2DL4(KIR)和 PRF1。狼疮疾病活动通过 SLEDAI 来确定。通过回归分析比较了男性和女性之间遗传评分、T 细胞 DNA 去甲基化与 SLEDAI 评分之间的相互作用。对每位患者的 DNA 去甲基化程度与遗传风险评分相结合的结果表明,狼疮患者的(遗传风险)/(DNA 甲基化)比值与疾病活动直接相关。重要的是,男性需要更大的(遗传风险)/(DNA 甲基化)比值才能达到与女性相当的 SLEDAI 评分(KIR 为 P = 0.010,PRF1 为 P = 0.0054)。这一差异不能仅用遗传风险或 T 细胞 DNA 去甲基化的差异来解释,这表明存在遗传-表观遗传相互作用。这些结果表明,遗传风险和 T 细胞 DNA 去甲基化在狼疮患者中相互作用,影响狼疮发作的严重程度,而男性需要更高的遗传风险和/或更大程度的 T 细胞 DNA 去甲基化才能达到与女性相当严重的狼疮发作。