Pathogenesis of cutaneous lupus erythema associated with and without systemic lupus erythema
Pathogenesis of cutaneous lupus erythema associated with and without systemic lupus erythema
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伴有或不伴有系统性红斑狼疮的皮肤红斑狼疮的发病机制
DOI：
10.1016/j.autrev.2017.05.009
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发表时间：
2017
影响因子：
13.6
通讯作者：
Wang Liangchun
中科院分区：
文献类型：
--
作者：
Zhang Yu-ping;Wu Jian;Han Yan-fang;Shi Zhen-rui;Wang Liangchun
皮肤红斑狼疮（CLE）可以是一种仅累及皮肤的个体疾病，也可以是SLE的一部分表现。一小部分CLE可能进展为SLE，然而，潜在的致病介质仍然难以捉摸。通过仅纳入明确描述入组受试者呈现的CLE亚型是否与SLE相关的研究，我们提供了血液和皮肤中鉴定的可能参与狼疮皮肤损伤的抗体、炎性细胞和炎性分子介质的概述。IgG自身抗体对于SLE相关CLE的发展至关重要，但循环中的炎性细胞和分子介质需要进一步研究以提供其与皮肤损伤相关的确切证据。盘状红斑狼疮（DLE）是CLE最常见的亚型。对于无SLE相关性的DLE（CDLE），自身抗体和循环炎性细胞是否参与其发病机制尚缺乏证据，但与SLE的多种复杂特征相比，皮肤炎性浸润明显以Th1细胞为主，而非Th17细胞。角质形成细胞作为皮肤的主要靶细胞，可能通过增加细胞凋亡和促炎细胞因子的产生参与SLE和CDLE的病理生理过程。了解CLE和SLE相关CLE的发病机制的相似性和差异也将改善我们目前从SLE开始采用的CLE治疗策略，并通过在疾病发展的适当窗口内提供干预措施来预防CLE向SLE的进展。
Cutaneous lupus erythematosus (CLE) can be an individual disease only involving skin, or presents as part of the manifestations of SLE. A small proportion of CLE may progress into SLE, however, the underlying pathogenic mediators remain elusive. By only including researches that clearly described if the subtypes of CLE presented by enrolled subjects was associated with or without SLE, we provided an overview of antibodies, inflammatory cells and inflammatory molecular mediators identified in blood and skin that were possibly involved in lupus skin damages. IgG autoantibodies are crucial for the development of CLE associated with SLE, but the circulating inflammatory cells and molecular mediators require further studies to provide definitive proof for their association with skin damages. Discoid lupus erythematosus (DLE) is the most common subtype of CLE. For DLE without associated with SLE (CDLE), it is lack of evidences if autoantibodies and circulating inflammatory cells are involved in the pathogenesis or not, but is clear that the cutaneous inflammatory infiltrates are dominated by Th1, but not Th17 cells in contrast to the various complex profile in SLE. As the major target cells in skin, keratinocytes may participate the pathophysiological process by increase cell apoptosis and the production of proinflammatory cytokines in SLE and CDLE. Insights into the similarities and differences of the pathogenesis of CLE and CLE associated with SLE will also improve our therapeutic strategies for CLE that is currently adopted from SLE, and prevent the progression of CLE to SLE by providing interventions within an appropriate window of disease development.