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补体在斑秃发病机制中起作用吗?

Does Complement Have a Role in the Pathogenesis of Alopecia Areata?

作者信息

Juhász Margit L W, Atanaskova Mesinkovska Natasha

机构信息

Department of Dermatology, University of California, Irvine, Irvine, California, USA.

出版信息

Skin Appendage Disord. 2018 Oct;4(4):261-263. doi: 10.1159/000487448. Epub 2018 Mar 22.

Abstract

Alopecia areata (AA) is an autoimmune disorder in which immune attack of the anagen follicle causes hair loss in approximately 2% of the population. Although the pathogenesis of AA has not been fully determined, most likely it is mediated by a variety of factors including cellular/humoral immunity and genetic predisposition. Researchers have been interested in the possible role of the complement pathway in AA since the 1970s. Given recent evidence suggesting that complement plays a role in many immunologic and inflammatory dermatologic diseases including systemic lupus erythematosus, bullous diseases, angioedema, lipodystrophy, and skin infections, it is likely that complement also contributes to AA pathogenesis. Although early serum studies and immunohistochemical staining have been unimpressive, recent genetics studies may provide evidence that complement does indeed contribute to AA. By determining if complement plays a role in AA, options for novel targeted treatments will become available for those patients with refractory disease.

摘要

斑秃(AA)是一种自身免疫性疾病,生长期毛囊的免疫攻击导致约2%的人群脱发。尽管AA的发病机制尚未完全明确,但很可能是由多种因素介导的,包括细胞/体液免疫和遗传易感性。自20世纪70年代以来,研究人员一直对补体途径在AA中可能发挥的作用感兴趣。鉴于最近有证据表明补体在许多免疫性和炎症性皮肤病中起作用,包括系统性红斑狼疮、大疱性疾病、血管性水肿、脂肪营养不良和皮肤感染,补体很可能也参与了AA的发病机制。尽管早期的血清学研究和免疫组织化学染色结果并不理想,但最近的遗传学研究可能会提供证据表明补体确实参与了AA的发病。通过确定补体是否在AA中起作用,对于那些难治性疾病患者将有新的靶向治疗选择。

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Does Complement Have a Role in the Pathogenesis of Alopecia Areata?补体在斑秃发病机制中起作用吗?
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本文引用的文献

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Complement system in dermatological diseases - fire under the skin.皮肤疾病中的补体系统——皮下之火。
Front Med (Lausanne). 2015 Jan 29;2:3. doi: 10.3389/fmed.2015.00003. eCollection 2015.
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Complement and its receptors: new insights into human disease.补体及其受体:对人类疾病的新认识。
Annu Rev Immunol. 2014;32:433-59. doi: 10.1146/annurev-immunol-032713-120154. Epub 2014 Jan 29.

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