雌激素受体与系统性红斑狼疮的关系  

The relationship between estrogen receptors and systemic lupus erythematosus

作　　者：李晓岚[1] 

机构地区：[1]昆明医学院第二附属医院皮肤性病风湿免疫科,650101

出　　处：《国际免疫学杂志》2009年第5期395-399,共5页International Journal of Immunology

基　　金：美国国立卫生研究院基金资助项目（NIH-2R15AI49272）

摘　　要：系统性红斑狼疮（SLE）发病机理涉及免疫系统自身识别的丧失，较易发生于生育期女性。雌激素对SLE的发病及病情发展有重要影响。雌激素通过与T、B细胞核内表达的雌激素受体ER-α和ER-β结合进而刺激或调节特异性免疫相关基因的转录。受体结构以及与靶基因相互作用的差异造成了雌激素的异常活动，使得对自身抗原耐受起重要作用的一系列调节通路紊乱，从而导致自身免疫病如SLE的发生。多种经典和非经典雌激素信号的传导通路在转录和转录后水平均调控T细胞活化基因的表达，造成SLE患者的T细胞对雌激素应答的敏感性差异。The pathogenesis of systemic lupus erythematosus （SLE） is a multifactorial event which includes the loss of self recognition, or autoimmunity. SLE occurs more frequently in women of reproductive age. Much evidence showed that estrogen is responsible for SLE onset and development. Estrogen binds to estrogen receptors, ER-α and ER-β, expressed in the nucleius of target, cells, such as T cells and B cells to stimulate or regulate the transcription of specific immune genes. The alteration in receptor structure and the interaction with target genes may underlie abnormal estrogen action, resulting in the disruption of regulatory pathways that are important in the maintenance of tolerance to self antigens and lead to the pathogenesis of autoimmune disorders including SLE. Several classical/ non-classical signal transduction pathways contribute to the differential sensitivity of SLE T cells to estrogen by regulating gene expression of T cell activation at transcriptional/posttranscriptional levels.

关 键 词：系统性红斑狼疮 雌激素 雌激素受体 雌激素受体Α 雌激素受体Β 

分 类 号：R593.241[医药卫生—内科学] R737.9[医药卫生—临床医学]