期刊文献+

黑色素瘤缺乏因子2与银屑病关系的研究进展 被引量:4

Research advances in correlation between absent in melanoma 2 and psoriasis
下载PDF
导出
摘要 银屑病是一种慢性自身免疫性炎症性皮肤病,其发病机制目前尚未完全阐明。黑色素瘤缺乏因子2(AIM2)是一种参与天然免疫的感受器,可识别双链脱氧核糖核酸(dsDNA)并进一步组装成为AIM2炎症小体。AIM2炎症小体是一种蛋白质复合体,然而AIM2对胞质自身脱氧核糖核酸(DNA)的不正确识别可导致银屑病、特应性皮炎、关节炎等自身免疫性和炎症性疾病的发生与发展,故抑制AIM2炎症小体激活有望成为银屑病的治疗新靶点。现将AIM2在银屑病中的作用机制和实验模型中AIM2炎症小体在银屑病中作用的证据综述如下。 Psoriasis is chronic autoimmune inflammatory skin disease and its pathogenesis has not been fully understood.Absent in melanoma 2(AIM2)is a sensor involved in innate immune response,can recognize double stranded deoxyribonucleic acid(dsDNA)and further assemble them into AIM2 inflammosome.AIM2 inflammasome is a protein complex,while inappropriate recognition of cytoplasmic self-DNA by AIM2 contributes to the development of psoriasis,atopic dermatitis,arthritis and other autoimmune as well as inflammatory diseases.Therefore,inhibition of AIM2 inflammasome activation is expected to be a new therapeutic target for psoriasis.This article reviewed the mechanism of AIM2 in psoriasis and the evidence of AIM2 inflammasome involving in the pathogenesis of experimental psoriasis model.
作者 梁黛雯 王丽雅 朱晓芳 LIANG Daiwen;WANG Liya;ZHU Xiaofang(Second Xiangya Hospital of Central South University,Changsha,Hunan,410011;Medical College,Yangzhou University,Yangzhou,Jiangsu,225001;Department of Dermatology,Clinical Medical College of Yangzhou University,Yangzhou,Jiangsu,225001)
出处 《实用临床医药杂志》 CAS 2021年第2期122-124,共3页 Journal of Clinical Medicine in Practice
基金 江苏省扬州市科技计划项目-社会发展(YZ2018065)。
关键词 黑色素瘤缺乏因子2 银屑病 焦亡 炎症小体 absent in melanoma 2 psoriasis pyroptosis inflammasone
  • 相关文献

参考文献5

二级参考文献23

  • 1Zhang C, Zhu K J, Liu H, et al. The TNFAIP3 polymorphism rs610604 both associates with the risk of psoriasis vulgaris and af- fects the clinical severity[ J]. Clin Exp Dermatol, 2015, 40 (4) :426 -30.
  • 2Boehneke W H. Etiology and pathogenesis of psoriasis[J]. Rheu- matic Dis Clin North Am, 2015, 41 (4) : 665 -75.
  • 3Zuo X B, Sun L D, Yin X Y, et al. Whole-exome SNP mTay i- dentifies 15 new susceptibility loci for psoriasis[ J]. Nat Commun, 2015, 6:6793.
  • 4Revicki D A, Jin Y, Wilson H D, et al. Reliability and validity of the psoriasis symptom inventory in patients with moderate-to-severe psoriasis[ J]. J Dermatolog Treat, 2014, 25 ( 1 ) :8 - 14.
  • 5Klein R J. Complement Factor H Polymorphism in Age-Related Macular Degeneration [ J ]. Science, 2005,308 (5720) : 385 - 9.
  • 6Ponomareva L, Liu H, Duan X, et al. AIM2, an IFN-indueible eytosolie DNA sensor, in the development of benign prostate hy- perplasia and prostate cancer [ J ]. Mol Cancer Res, 2013, 11 (10) :1193 -202.
  • 7Biirekstiimmer T, Baumann C, Bltiml S, et al. An orthogonal pro- teomie-genmnic screen identifies AIM2 as a cytoplasmic DNA sen- sor for the inflammasome [ J ]. Nat Inmmn, 2009, 10 ( 3 ) :266 - 72.
  • 8Jin T, Perry A, Smith P, et al. Structure of the absent in melano- ma 2 (AIM2) pyrin domain provides insights into the mechanisms of AIM2 autoinhibition and inflammasome assembly [ J ]. J Bio Chem, 2013,288 ( 19 ) : 13225 - 35.
  • 9Kopfnagel V, Wittmann M, Werfel T. Human keratinoeytes ex- press AIM2 and respond to dsDNA with IL-113 secretion[ J]. Exp Delatol, 2011, 20(12):1027-29.
  • 10Xie C, Mao X, Huang J, et al. KOBAS 2.0 : a web server for an- notation and identification of enriched pathways and diseases[ J ]. Nucleic Acids Res, 2011, 39(Suppl 2) :W316 -22.

共引文献24

同被引文献48

引证文献4

二级引证文献11

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部