共 1 条
[1]
Yasuda K, 2019, SEMIN IMMUNOPATHOL, V41, P283, DOI 10.1007/s00281-019-00733-8
The pathogenicity of Th17 cells in autoimmune diseases (vol 41, pg 283, 2019)
被引：125
作者：
Yasuda, Keiko
[1
,2
]
Takeuchi, Yusuke
[1
,3
]
Hirota, Keiji
[1
]
机构：
[1] Kyoto Univ, Inst Frontier Life & Med Sci, Lab Integrat Biol Sci, Kyoto 6068507, Japan
[2] Osaka Univ, Grad Sch Med, Dept Nephrol, Osaka, Japan
[3] Kyoto Univ, Grad Sch Med, Dept Rheumatol & Clin Immunol, Kyoto, Japan
关键词：
Autoimmune arthritis;
EAE;
GM-CSF;
IL-17;
Rheumatoid arthritis;
Th17;
cells;
D O I：
10.1007/s00281-019-00746-3
中图分类号：
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
IL-17-producing T helper (Th17) cells have been implicated in the pathogenesis of many inflammatory and autoimmune diseases. Targeting the effector cytokines IL-17 and GM-CSF secreted by autoimmune Th17 cells has been shown to be effective for the treatment of the diseases. Understanding a molecular basis of Th17 differentiation and effector functions is therefore critical for the regulation of the pathogenicity of tissue Th17 cells in chronic inflammation. Here, we discuss the roles of proinflammatory cytokines and environmental stimuli in the control of Th17 differentiation and chronic tissue inflammation by pathogenic Th17 cells in humans and in mouse models of autoimmune diseases. We also highlight recent advances in the regulation of pathogenic Th17 cells by gut microbiota and immunometabolism in autoimmune arthritis. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.
引用
收藏
页码：299 / 299
页数：1
相关论文