Systemic lupus erythematosus flares when genetically predisposed people encounter environmental agents that cause oxidative stress, such as infections and sunlight. How these modify the immune system to initiate flares is unclear. Drug induced lupus models demonstrate that CD4+ T cells epigenetically altered with DNA methylation inhibitors cause lupus in animal models, and similar T cells are found in patients with active lupus. How infections and sun exposure inhibit T cell DNA methylation is unclear. DNA methylation patterns are replicated each time a cell divides in a process that requires DNA methyltransferase one (Dnmt1), which is upregulated as cells enter mitosis, as well as the methyl donor S-adenosylmethionine, created from dietary sources. Reactive oxygen species that inhibit Dnmt1 upregulation, and a diet poor in methyl donors, combine to cause lupus in animal models. Similar changes are found in patients with active lupus, indicating a mechanism contributing to lupus flares.

当遗传上易患疾病的人遇到引起氧化应激（例如感染和阳光）的环境因素时，系统性红斑狼疮会发作。这些如何改变免疫系统引发耀斑尚不清楚。药物诱发的狼疮模型表明，在动物模型中，被DNA甲基化抑制剂表观遗传改变的CD4 + T细胞引起了狼疮，在活动性狼疮患者中也发现了类似的T细胞。感染和日晒如何抑制T细胞DNA甲基化尚不清楚。每次细胞分裂都会复制DNA甲基化模式，该过程需要DNA甲基转移酶1（Dnmt1）（随着细胞进入有丝分裂而被上调），以及从饮食来源产生的甲基供体S-腺苷甲硫氨酸。抑制Dnmt1上调的活性氧，饮食中甲基供体含量低，合并在动物模型中引起狼疮。在患有活动性狼疮的患者中发现了类似的变化，这表明促成狼疮发作的机制。