Hypomorphic A20 expression confers susceptibility to psoriasis

被引：20

作者：

Aki, Anri ^{[1
]}

Nagasaki, Miyuki ^{[1
]}

Malynn, Barbara Ann ^{[2
]}

Ma, Averil ^{[2
]}

Kagari, Takashi ^{[1
]}

机构：

[1] Daiichi Sankyo Co Ltd, R&D Div, Oncol Funct, Biol & Immunooncol Labs, Tokyo, Japan

[2] Univ Calif San Francisco, Dept Med, San Francisco, CA USA

来源：

PLOS ONE | 2017年 / 12卷 / 06期

基金：

美国国家卫生研究院;

关键词：

NF-KAPPA-B; MODIFYING ENZYME A20; RESTRICTS UBIQUITINATION; INHIBITION; CELLS; PROTEIN; INTERLEUKIN-17; INFLAMMATION; REVEALS; ABSENCE;

D O I：

10.1371/journal.pone.0180481

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];

摘要：

Psoriasis is a common inflammatory skin disease that affects approximately 1% of the population worldwide. Tumor necrosis factor-alpha-induced protein 3 (TNFAIP3) gene polymorphisms have been strongly associated with psoriasis susceptibility. In this study, we investigate how TNFAIP3, also known as A20, may regulate psoriasis susceptibility. We found that haplo-insufficient A20(+/-) mice develop severe toll-like receptor (TLR)-induced skin inflammation compared to wild type mice owing to amplified production of interleukin (IL)-17 and IL-23. Examination of TNFAIP3 mRNA expression in skin biopsies from patients with psoriasis revealed reduced expression in both involved and uninvolved skin. Our results demonstrate the clinical importance of reduced dermal expression of A20 in psoriasis and suggest that A20 restriction of the IL-23/17 axis protects against psoriasis.

引用

页数：14

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