IL-17在类风湿性关节炎发病机制中的作用

被引：34

作者：

卢月 ^{[1
]}

曹雅晶 ^{[2
]}

钱瑞琴 ^{[1
]}

机构：

[1] 北京大学医学部基础医学院中西医结合教研室

[2] 北京大学医学部基础医学院

来源：

中国免疫学杂志 | 2011年 / 27卷 / 09期

基金：

北京市自然科学基金;

关键词：

D O I：

暂无

中图分类号：

R593.22 [类风湿性关节炎];

学科分类号：

100201 [内科学];

摘要：

<正>类风湿性关节炎(RA)是一种以滑膜持续炎症和关节软骨及骨破坏为特征的自身免疫性疾病。RA的发展伴随着滑膜细胞增生、新生血管形成,以及局部大量T细胞浸润[1]。IL-17是主要由Th17细

引用

页码：855 / 859

页数：5

共 9 条

[1]

Th17 cytokines and arthritis [J].

Lubberts, Erik .

SEMINARS IN IMMUNOPATHOLOGY, 2010, 32 (01) :43-53

[2]

Differential Roles of Interleukin-17A and-17F in Host Defense against Mucoepithelial Bacterial Infection and Allergic Responses [J].

Ishigame, Harumichi ;

Kakuta, Shigeru ;

Nagai, Takeshi ;

Kadoki, Motohiko ;

Nambu, Aya ;

Komiyama, Yutaka ;

Fujikado, Noriyuki ;

Tanahashi, Yuko ;

Akitsu, Aoi ;

Kotaki, Hayato ;

Sudo, Katsuko ;

Nakae, Susumu ;

Sasakawa, Chihiro ;

Iwakura, Yoichiro .

IMMUNITY, 2009, 30 (01) :108-119

[3]

IL-17F: Regulation, signaling and function in inflammation [J].

Chang, Seon Hee ;

Dong, Chen .

CYTOKINE, 2009, 46 (01) :7-11

[4]

Th17 T cells: Linking innate and adaptive immunity [J].

Stockinger, Brigitta ;

Veldhoen, Marc ;

Martin, Bruno .

SEMINARS IN IMMUNOLOGY, 2007, 19 (06) :353-361

[5]

Presentation of arthritogenic peptide to antigen-specific T cells by fibroblast-like synoviocytes [J].

Tran, Chinh N. ;

Davis, Michael J. ;

Tesmer, Laura A. ;

Endres, Judith L. ;

Motyl, Christopher D. ;

Smuda, Craig ;

Somers, Emily C. ;

Chung, Kevin C. ;

Urquhart, Andrew G. ;

Lundy, Steven K. ;

Kovats, Susan ;

Fox, David A. .

ARTHRITIS AND RHEUMATISM, 2007, 56 (05) :1497-1506

[6]

IL-17 Family Cytokines and the Expanding Diversity of Effector T Cell Lineages.[J].Casey T. Weaver;Robin D. Hatton;Paul R. Mangan;Laurie E. Harrington.Annual Review of Immunology.2007, 0

[7]

IL-17 increased the production of vascular endothelial growth factor in rheumatoid arthritis synoviocytes.[J].S. Ryu;J. H. Lee;S. I. Kim.Clinical Rheumatology.2005, 1

[8]

IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritis [J].