Role of IL-17 family cytokines in the progression of IPF from inflammation to fibrosis

被引:7
作者
YunJuan Nie [1 ]
ShuoHua Wu [2 ]
YingHua Xuan [3 ]
Gen Yan [4 ]
机构
[1] Department of Basic Medicine,Wuxi School of Medicine,Jiangnan University
[2] Department of Radiology,the Second Affiliated Hospital,Medical College of Shantou University
[3] Department of Basic Medicine,Xiamen Medical College
[4] Department of Radiology,the Second Affiliated Hospital of Xiamen Medical College
关键词
D O I
暂无
中图分类号
R563 [肺疾病];
学科分类号
1002 ; 100201 ;
摘要
Idiopathic pulmonary fibrosis(IPF) is a fatal chronic interstitial lung disease with no established treatment and is characterized by progressive scarring of the lung tissue and an irreversible decline in lung function. Chronic inflammation has been demonstrated to be the pathological basis of fibrosis. Emerging studies have revealed that most interleukin-17(IL-17) isoforms are essential for the mediation of acute and chronic inflammation via innate and adaptive immunity. Overexpression or aberrant expression of IL-17 cytokines contributes to various pathological outcomes, including the initiation and exacerbation of IPF. Here, we aim to provide an overview of IL-17 family members in the pathogenesis of IPF.
引用
收藏
页码:618 / 627
页数:10
相关论文
共 62 条
[31]  
Brodalumab, an Anti-IL17RA Monoclonal Antibody, in Psoriatic Arthritis[J] . Philip J. Mease,Mark C. Genovese,Maria W. Greenwald,Christopher T. Ritchlin,André D. Beaulieu,Atul Deodhar,Richard Newmark,JingYuan Feng,Ngozi Erondu,Ajay Nirula.The New England Journal of Medicine . 2014 (24)
[32]  
IL-33 promotes ST2-dependent lung fibrosis by the induction of alternatively activated macrophages and innate lymphoid cells in mice[J] . Dong Li,Rodrigo Guabiraba,Anne-Ga?lle Besnard,Mousa Komai-Koma,Majid S. Jabir,Li Zhang,Gerard J. Graham,Mariola Kurowska-Stolarska,Foo Y. Liew,Charles McSharry,Damo Xu.The Journal of Allergy and Clinical Immunology . 2014
[33]   Neutrophils produce interleukin-17B in rheumatoid synovial tissue [J].
Kouri, Vesa-Petteri ;
Olkkonen, Juri ;
Ainola, Mari ;
Li, Tian-Fang ;
Bjorkman, Lena ;
Konttinen, Yrjo T. ;
Mandelin, Jami .
RHEUMATOLOGY, 2014, 53 (01) :39-47
[34]   IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis [J].
Hams, Emily ;
Armstrong, Michelle E. ;
Barlow, Jillian L. ;
Saunders, Sean P. ;
Schwartz, Christian ;
Cooke, Gordon ;
Fahy, Ruairi J. ;
Crotty, Thomas B. ;
Hirani, Nikhil ;
Flynn, Robin J. ;
Voehringer, David ;
McKenzie, Andrew N. J. ;
Donnelly, Seamas C. ;
Fallon, Padraic G. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2014, 111 (01) :367-372
[35]   IL-17 family cytokines mediated signaling in the pathogenesis of inflammatory diseases [J].
Song, Xinyang ;
Qian, Youcun .
CELLULAR SIGNALLING, 2013, 25 (12) :2335-2347
[36]   IL-17 targeted therapies for psoriasis [J].
Chiricozzi, Andrea ;
Krueger, James G. .
EXPERT OPINION ON INVESTIGATIONAL DRUGS, 2013, 22 (08) :993-1005
[37]   Interleukin 17A inhibits autophagy through activation of PIK3CA to interrupt the GSK3B-mediated degradation of BCL2 in lung epithelial cells [J].
Liu, Hong ;
Mi, Su ;
Li, Zhe ;
Hua, Fang ;
Hu, Zhuo-Wei .
AUTOPHAGY, 2013, 9 (05) :730-742
[38]  
STAT3: a central mediator of pulmonary fibrosis?[J] . Prêle Cecilia M,Yao Eric,O’Donoghue Robert J J,Mutsaers Steven E,Knight Darryl A.Proceedings of the American Thoracic Society . 2012 (3)
[39]   IL-17C regulates the innate immune function of epithelial cells in an autocrine manner [J].
Ramirez-Carrozzi, Vladimir ;
Sambandam, Arivazhagan ;
Luis, Elizabeth ;
Lin, Zhongua ;
Jeet, Surinder ;
Lesch, Justin ;
Hackney, Jason ;
Kim, Janice ;
Zhou, Meijuan ;
Lai, Joyce ;
Modrusan, Zora ;
Sai, Tao ;
Lee, Wyne ;
Xu, Min ;
Caplazi, Patrick ;
Diehl, Lauri ;
de Voss, Jason ;
Balazs, Mercedesz ;
Gonzalez, Lino, Jr. ;
Singh, Harinder ;
Ouyang, Wenjun ;
Pappu, Rajita .
NATURE IMMUNOLOGY, 2011, 12 (12) :1159-U46
[40]   Functional Specialization of Interleukin-17 Family Members [J].
Iwakura, Yoichiro ;
Ishigame, Harumichi ;
Saijo, Shinobu ;
Nakae, Susumu .
IMMUNITY, 2011, 34 (02) :149-162