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银屑病免疫发病机制的当前概念

Current concepts in the immunopathogenesis of psoriasis.

作者信息

Lowes Michelle A, Lew Wook, Krueger James G

机构信息

Rockefeller University, 1230 York Avenue, Box 178, New York, NY 10021, USA.

出版信息

Dermatol Clin. 2004 Oct;22(4):349-69, vii. doi: 10.1016/j.det.2004.03.010.

Abstract

There is much evidence to support the concept that psoriasis is a type 1 autoimmune disease, primarily mediated by interferon gamma and other inflammatory cytokines. There has been renewed interest in the role of components of the innate immune system, however,and it may be that overlap between the innate and acquired arms of the immune system can better explain immunopathogenesis in psoriasis. Relevant cell types, receptors, and immune mediators within these traditional boundaries of the immune system are discussed.Finally, pathogenic contributions from important psoriatic mouse models and recent genomic data using the new gene chip technology are elaborated.

摘要

有大量证据支持银屑病是一种1型自身免疫性疾病的概念,主要由干扰素γ和其他炎性细胞因子介导。然而,人们对固有免疫系统组成部分的作用重新产生了兴趣,免疫系统的固有和后天分支之间的重叠可能能更好地解释银屑病的免疫发病机制。本文讨论了免疫系统这些传统范畴内的相关细胞类型、受体和免疫介质。最后,阐述了重要的银屑病小鼠模型以及使用新基因芯片技术的最新基因组数据所产生的致病作用。

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