Th17/Th1细胞及相关细胞因子在银屑病关节炎中的研究进展

被引:5
作者
王泉丽 [1 ]
张改连 [2 ]
张莉芸 [2 ]
机构
[1] 山西医科大学研究生院
[2] 山西医学科学院山西大医院风湿科
关键词
D O I
暂无
中图分类号
R758.63 [牛皮癣(银屑病)];
学科分类号
100227 [皮肤病学];
摘要
<正>银屑病关节炎(psoriasis arthritis,PsA)又称关节病型银屑病,是银屑病的一种特殊类型,在银屑病患者中的发病率为6%42%[1]。其病因尚不清楚,涉及遗传、免疫调节、环境及精神等多种因素。对本病发病机制的研究一直是国内外学者研究的热点,但至今尚未得出明确的结论。近年来越来越多的研究证实,免疫学异常在其发病中起着核心作用。Th1、Th17细胞及其相关细胞因子对PsA发生、发展的作用备受关注。1 Th1细胞Th1细胞曾被认为是PsA主要的致病性T细胞。以往研究表明,与健康人皮肤相比银屑病皮损处以Th1型细胞因子白细胞介素(IL)-2、干扰素-γ、肿瘤坏死因子(TNF)-α表达为主,而Th2型细胞因子IL-4、IL-5、IL-10则表达减少[2]。在银屑
引用
收藏
相关论文
共 12 条
[1]
银屑病性关节炎患者Th17/Treg相关细胞因子的检测 [J].
陈晋广 ;
姜昱 .
中国皮肤性病学杂志, 2012, 26 (11) :969-970+976
[2]
寻常性银屑病患者外周血Th1和Th17细胞亚群的研究 [J].
钟道清 ;
罗育武 ;
罗权 .
广州医药, 2012, 43 (03) :16-18
[3]
Th17细胞及其与银屑病关系的研究 [J].
沈燕芸 ;
徐金华 .
中国麻风皮肤病杂志, 2009, 25 (05) :361-363
[4]
The Th17/IL-23 Axis and Natural Immunity in Psoriatic Arthritis[J] Shinji Maeda;Yoshihito Hayami;Taio Naniwa;Ryuzo Ueda;Lazaros I. Sakkas International Journal of Rheumatology 2012,
[5]
The IL‐17 pathway as a major therapeutic target in autoimmune diseases[J] YanHu;FangShen;Natasha K.Crellin;WenjunOuyang Annals of the New York Academy of Sciences 2011,
[6]
Immunological aspect of cardiac remodeling: T lymphocyte subsets in inflammation-mediated cardiac fibrosis[J] Liu Wei Experimental and Molecular Pathology 2010,
[7]
Ustekinumab improves health‐related quality of life in patients with moderate‐to‐severe psoriasis: results from the PHOENIX 1 trial[J] M.Lebwohl;K.Papp;C.Han;B.Schenkel;N.Yeilding;Y.Wang;G.G.Krueger British Journal of Dermatology 2009,
[8]
Ustekinumab; a human interleukin 12/23 monoclonal antibody; for psoriatic arthritis: randomised; double-blind; placebo-controlled; crossover trial[J] Alice Gottlieb;Alan Menter;Alan Mendelsohn;Yaung-Kaung Shen;Shu Li;Cynthia Guzzo;Scott Fretzin;Rod Kunynetz;Arthur Kavanaugh The Lancet 2009,
[9]
Keratinocyte but Not Endothelial Cell-Specific Overexpression of Tie2 Leads to the Development of Psoriasis[J] Julie A. Wolfram;Doina Diaconu;Denise A. Hatala;Jessica Rastegar;Dorothy A. Knutsen;Abigail Lowther;David Askew;Anita C. Gilliam;Thomas S. McCormick;Nicole L. Ward The American Journal of Pathology 2009,
[10]
Interleukin‐1 drives pathogenic Th17 cells during spontaneous arthritis in interleukin‐1 receptor antagonist–deficient mice[J] Marije I.Koenders;IsabelDevesa;Renoud J.Marijnissen;ShahlaAbdollahi‐Roodsaz;Annemieke M. H.Boots;BirgitteWalgreen;Franco E.di Padova;Martin J. H.Nicklin;Leo A. B.Joosten;Wim B.van den Berg Arthritis & Rheumatism 2008,