EVIDENCE FOR IMPAIRED T-CELL DNA METHYLATION IN SYSTEMIC LUPUS-ERYTHEMATOSUS AND RHEUMATOID-ARTHRITIS
EVIDENCE FOR IMPAIRED T-CELL DNA METHYLATION IN SYSTEMIC LUPUS-ERYTHEMATOSUS AND RHEUMATOID-ARTHRITIS
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DOI：
10.1002/art.1780331109
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发表时间：
1990-11-01
影响因子：
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通讯作者：
JOHNSON, M
中科院分区：
文献类型：
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作者：
RICHARDSON, B;SCHEINBART, L;JOHNSON, M
普鲁卡因酰胺和肼苯哒嗪抑制T细胞DNA甲基化并诱导克隆的CD4+ T细胞中的自身反应性。这些药物还诱导自身免疫综合征，表明DNA低甲基化，T细胞自身反应性和某些自身免疫性疾病之间可能存在关系。为了检验这种关系，研究人员在类风湿性关节炎和系统性红斑狼疮患者的T细胞中研究了DNA甲基化，发现DNA甲基化受损。这些结果支持DNA低甲基化和某些形式的自身免疫性疾病之间的关系。
Procainamide and hydralazine inhibit T cell DNA methylation and induce autoreactivity in cloned CD4+ T cells. These drugs also induce an autoimmune syndrome, suggesting a possible relationship between DNA hypomethylation, T cell autoreactivity, and certain autoimmune diseases. To test this relationship, DNA methylation was studied in T cells from patients with rheumatoid arthritis and patients with systemic lupus erythematosus, and was found to be impaired. These results support a relationship between DNA hypomethylation and some forms of autoimmune disease.