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皮肤红斑狼疮中与I型干扰素相关的细胞毒性炎症

Type I interferon-associated cytotoxic inflammation in cutaneous lupus erythematosus.

作者信息

Wenzel Joerg, Zahn Sabine, Bieber Thomas, Tüting Thomas

机构信息

Department of Dermatology, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany.

出版信息

Arch Dermatol Res. 2009 Jan;301(1):83-6. doi: 10.1007/s00403-008-0892-8. Epub 2008 Sep 11.

Abstract

Inappropriate activation of innate immune mechanisms, in particular of the type I interferon (IFN) system, is regarded to play an important role in the pathogenesis of lupus erythematosus (LE). Type I IFN serum levels have been shown to correlate with the disease activity in systemic LE and additionally play a proinflammatory role in the development of LE skin lesions. Recent studies demonstrated a close morphological association between the expression pattern of IFN-inducible chemokines (MxA, CXCL10) and typical histological features of cutaneous LE. These and other studies suggest that a complex network of IFN-associated cytokines, chemokines and adhesion molecules orchestrates and promotes tissue injury observed in LE skin.

摘要

先天性免疫机制,特别是I型干扰素(IFN)系统的不适当激活,被认为在红斑狼疮(LE)的发病机制中起重要作用。I型干扰素血清水平已被证明与系统性红斑狼疮的疾病活动相关,并且在红斑狼疮皮肤病变的发展中还发挥促炎作用。最近的研究表明,IFN诱导的趋化因子(MxA、CXCL10)的表达模式与皮肤型红斑狼疮的典型组织学特征之间存在密切的形态学关联。这些研究以及其他研究表明,一个由IFN相关细胞因子、趋化因子和黏附分子组成的复杂网络,共同协调并促进了红斑狼疮皮肤中观察到的组织损伤。

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