期刊文献+

银屑病中主要免疫细胞和相关细胞因子的研究进展 被引量:31

Progress of Research on Main Immune Cells and Related Cytokines in Psoriasis
在线阅读 下载PDF
导出
摘要 银屑病是一种常见并易复发的慢性炎症性皮肤病。本病的确切病因尚未清楚,Th1和Th17介导的慢性炎症反应、表皮过度增殖和慢性新血管生成是目前被广泛认可的发病机制,阻断TNF-α和IL-23/Th17相关途径的生物制剂是迄今为止治疗银屑病最有效的药物。然而,尽管生物制剂治疗方面取得了较好的进展,但仍无法完全满足银屑病治疗上的需要,提示目前对银屑病潜在发病机制仍存在认识上的盲点。因此,本综述主要关注包括Th17细胞及其他参与银屑病发病机制的重要效应细胞(中性粒细胞、单核细胞和肥大细胞)以及相关细胞因子的研究进展,以便更全面了解银屑病的发病机制,为银屑病的治疗提供理论依据。 Psoriasis is a common and recurrent chronic inflammatory skin disease.The exact etiology of this disease is not clear.Th1 and Th17 mediated chronic inflammatory response,epidermal hyperproliferation and chronic neovascularization are widely recognized pathogenesis.Biological agents blocking TNF-αand IL-23/Th17 related pathways are the most effective drugs to treat psoriasis so far.However,despite the good progress in biological agent therapy,it still can not fully meet the needs of psoriasis treatment,suggesting that there is still a blind spot in understanding the potential pathogenesis of psoriasis.Therefore,this review mainly focuses on the research progress of Th17 cells and other important effector cells(neutrophils,monocytes and mast cells)and related cytokines involved in the pathogenesis of psoriasis,so as to understand the pathogenesis of psoriasis more comprehensively and provide theoretical basis for the treatment of psoriasis.
作者 陈雪琴 宋志强 CHEN Xueqin;SONG Zhiqiang(Department of Dermatology,First Hospital Affiliated to Army Military Medical University,Southwest Hospital,Chongqing 400038,China)
出处 《中国皮肤性病学杂志》 CAS CSCD 北大核心 2020年第11期1321-1325,共5页 The Chinese Journal of Dermatovenereology
基金 陆军军医大学西南医院创新团队培养计划(SWH2018TD-02)。
关键词 银屑病 发病机制 TH17 IL-17 Psoriasis Pathogenesis Th17 IL-17
作者简介 通信作者:宋志强,E-mail:zhiqiang.song@hotmail.com。
  • 相关文献

参考文献5

二级参考文献52

  • 1罗素菊,彭振辉,郑焱,张路坤,曹振平,王国荣.NB-UVB和阿维A对角质形成细胞肝素结合表皮生长因子样生长因子mRNA的影响[J].中华皮肤科杂志,2007,40(9):546-548. 被引量:2
  • 2Dardalhon V, Awasthi A, Kwon H, et al. IL-4 inhibits TGF-beta-induced Foxp3 + T cells and, together with TGF-beta, generates IL-9 + IL-10 + Foxp3 (-) effector T cells [ J ]. Nat Immunol, 2008,9 ( 12 ) : 1347-1355.
  • 3Veldhoen M, Uyttenhove C, van Snick J, et al. Transforming growth factor-beta ‘ reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset [ J ]. Nat Immunol, 2008,9(12) :1341-1346.
  • 4Jager A, Dardalhon V, Sobel RA, et al. Thl ,Th17, and Th9 effector ceils induce experimental autoimmune encephalomyelitis with different pathological phenotypes [ J ]. J Immunol, 2009,183 ( 11 ) : 7169-7177.
  • 5Li H, Nourbakhsh B, Cullimore M, et al. IL-9 is important for T- cell activation and differentiation in autoimmune inflammation of the central nervous system [ J]. Eur J Immunol, 2011,41 ( 8 ) : 2197-2206.
  • 6Ouyang H,Shi Y, Liu Z, et al. Increased interleukin 9 and CD4 ^+ IL-9 + T ceils in patients with systemic lupus erythematosus [ J ]. Mol Med Rep, 2013,7 ( 3 ) : 1031-1037.
  • 7Kaplan MH, Hufford MM, Olson MR. The development and in vivo function of T helper 9 cells [ J ]. Nat Rev Immunol, 2015,15 ( 5 ) : 295-307.
  • 8Cheng G, Yu A, Dee MJ, et al. IL-2R signaling is essential for functional maturation of regulatory T cells during thymic development[ J]. J Immunol, 2013,190 (4) : 1567-1575.
  • 9Van de Veerdonk FL, Netea MG. New Insights in the Immunobiology of IL-1 Family Members [ J ]. Front Immunol, 2013 Jul 8 ; 4 : 167.
  • 10Angkasekwinai P, Srimanote P, Wang YH, et al. Interleukin-25 ( IL- 25 ) promotes efficient protective immunity against Tfichinella spiralis infection by enhancing the antigen-specific IL-9 response[ J]. Infect Immun, 2013,81 ( 10 ) : 3731-3741.

共引文献42

同被引文献359

引证文献31

二级引证文献100

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