瘦素相关多态性与SLE

A. Cava
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引用次数: 3

摘要

瘦素是一种主要由脂肪细胞产生的激素/细胞因子,具有从控制代谢平衡到调节适应性和先天免疫反应的一系列作用。许多研究表明,瘦素的促炎活性可以显著促进和维持自身免疫反应。系统性红斑狼疮(SLE)是一种以多器官受累和自身抗体存在为特征的自身免疫性疾病,目前尚不清楚SLE患者瘦素的异常升高是否能反映该疾病的慢性炎症状态或有助于该疾病的发病机制。为了部分解决这个问题,最近的一项研究分析了来自不同祖先群体的大量SLE个体中瘦素相关基因多态性。该研究确定了与某些snp的弱关联,经过多次测试校正后,这些snp不再显著。这篇综述讨论了这些发现对SLE发病机制的影响,以及以瘦素为基础的疾病治疗干预方式的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Leptin-related polymorphisms and SLE
Leptin is a hormone/cytokine that is mainly produced by adipocytes and has a range of actions that span from the control of metabolic balance to the modulation of adaptive and innate immune responses. Many investigations have indicated that the pro-inflammatory activities of leptin can contribute significantly to the promotion and maintenance of autoimmune responses. It is not known whether the abnormal elevation of leptin in patients with systemic lupus erythematous (SLE) - an autoimmune disease characterized by multi-organ involvement and the presence of autoantibodies – can reflect the chronic inflammatory status of the disease or contributes to the pathogenesis of the disease. To partly address this question, a recent investigation analyzed several leptin-related gene polymorphisms in SLE in large numbers of individuals from different ancestral groups. The study identified weak associations with certain SNPs that did not remain significant after correction for multiple testing. This review discusses the implications of those findings for the pathogenesis of SLE and for the possibility of leptin-based modalities of therapeutic intervention in the disease.
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