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DNA低甲基化与系统性红斑狼疮关系的研究进展 被引量:7

Advances in research on relationship between DNA hypomethylation and systemic lupus erythematosus
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摘要 当各种原因引起T细胞DNA低甲基化后,对自身免疫有潜在作用的基因表达增加。CD 70过度表达可能与B细胞的活化、免疫球蛋白的分泌有关。perforin可能在T细胞介导的单核巨噬细胞凋亡中起重要作用。DNA低甲基化可使人类的内源性逆转录病毒序列活化,表达的抗原可以诱导机体产生自身抗体。多胺改变了染色体的正常结构,干扰了DNA的甲基化过程,在自身免疫性疾病中的发病作用近来引起了人们的关注。 T-cell DNA hypomethylation can increase expression of genes that have potential relation to autoimmunity. CD70 overexpression may be associated with B-cell activation and immunoglobulin secretion,while perforin plays an important role in T-cell-mediated macrophage apoptosis. DNA hypomethylation can activate human endogenous retroviruses (HERV) sequences. Expression of HERV components may elicit autoantibodies production. Polyamines change structure of chromosome and interfere with DNA methylation process,which is involved in the pathogenesis of autoimmune diseases.
作者 李尊忠 郑敏
出处 《浙江大学学报(医学版)》 CAS CSCD 2006年第4期458-462,共5页 Journal of Zhejiang University(Medical Sciences)
关键词 DNA甲基化 红斑狼疮 系统性/遗传学 内源性逆转录病毒 多胺 DNA methylation Lupus erythematosus, systemic/genet Human endogenous retroviruses Polyamine
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参考文献24

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二级参考文献34

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