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IL-17-producing ST2(+) group 2 innate lymphoid cells play a pathogenic role in lung inflammation

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作者：
Cai, Ting[1] * ; Qiu, Jinxin[1] * ; Ji, Yan[1] ; Li, Wenjing[2] ; Ding, Zhaoyun[1] ; Suo, Caixia[1] ; Chang, Jiali[1] ; Wang, Jingjing[1] ; He, Rui[2] ; Qian, Youcun[1] ; Guo, Xiaohuan[3,4] ; Zhou, Liang[5] ; Sheng, Huiming[6,*3] ; Shen, Lei[7,*2] ; Qiu, Ju[1,*1] ;
机构： [1]Chinese Acad Sci, Shanghai Inst Nutr & Hlth, CAS Key Lab Tissue Microenvironm & Tumor, Univ Chinese Acad Sci,Shanghai Inst Biol Sci, Shanghai, Peoples R China [2]Fudan Univ, Sch Basic Med Sci, Dept Immunol, Shanghai, Peoples R China [3]Tsinghua Univ, Inst Immunol, Beijing, Peoples R China [4]Tsinghua Univ, Dept Basic Med Sci, Sch Med, Beijing, Peoples R China [5]Univ Florida, Coll Vet Med, Dept Infect Dis & Immunol, Gainesville, FL USA [6]Shanghai Jiao Tong Univ, Sch Med, Tongren Hosp, Shanghai 200336, Peoples R China [7]Shanghai Jiao Tong Univ, Sch Med, Shanghai Key Lab Tumor Microenvironm & Inflammat, Shanghai Inst Immunol, Shanghai, Peoples R China
出处：
DOI： 10.1016/j.jaci.2018.03.007
ISSN：

关键词： Asthma group 2 innate lymphoid cells IL-17

摘要：
Background: IL-17 plays a pathogenic role in asthma. ST2(-) inflammatory group 2 innate lymphoid cells (ILC2s) driven by IL-25 can produce IL-17, whereas ST2(+) natural ILC2s produce little IL-17. Objective: We characterized ST2(+) IL-17(+) ILC2s during lung inflammation and determined the pathogenesis and molecular regulation of ST2(+)IL-17(+) ILC2s. Methods: Lung inflammation was induced by papain or IL-33. IL-17 production by lung ILC2s from wild-type, Rag1(-/-), Rorc(gfp/gfp), and aryl hydrocarbon receptor (Ahr)(-/-) mice was examined by using flow cytometry. Bone marrow transfer experiments were performed to evaluate hematopoietic myeloid differentiation primary response gene-88 (MyD88) signaling in regulating IL-17 production by ILC2s. mRNA expression of IL-17 was analyzed in purified naive ILC2s treated with IL-33, leukotrienes, and inhibitors for nuclear factor of activated T cells, p38, c-Jun N-terminal kinase, or nuclear factor kappa light-chain enhancer of activated B cells. The pathogenesis of IL-17(+) ILC2s was determined by transferring wild-type or Il17(-/-) ILC2s to Rag2(-/-) Il2rg(-/-) mice, which further induced lung inflammation. Finally, expression of 106 ILC2 signature genes was compared between ST2(+)IL-17(+) ILC2s and ST2(+)IL-17(-) ILC2s. Results: Papain or IL-33 treatment boosted IL-17 production from ST2(+) ILC2s (referred to by us as ILC2(17)s) but not ST2(-) ILC2s. Ahr, but not retinoic acid receptor-related orphan receptor gamma t, facilitated the production of IL-17 by ILC2(17)s. The hematopoietic compartment of MyD88 signaling is essential for ILC2(17) induction. IL-33 works in synergy with leukotrienes, which signal through nuclear factor of activated T-cell activation to promote IL-17 in ILC2(17)s. Il17(-/-) ILC2s were less pathogenic in lung inflammation. ILC2(17)s concomitantly expressed IL-5 and IL-13 but expressed little GM-CSF. Conclusion: During lung inflammation, IL-33 and leukotrienes synergistically induce ILC2(17)s. ILC2(17)s are a highly pathogenic and unexpected source for IL-17 in lung inflammation.

基金：
Ministry of Science and Technology of ChinaMinistry of Science and Technology, China [2015CB943400, 2014CB943300]; Strategic priority Research Program of the Chinese Academy of SciencesChinese Academy of Sciences [XDB19000000]; China's Youth 1000-Talent Program [91542102, 31570887]; Natural Science Foundation of ShanghaiNatural Science Foundation of Shanghai [16ZR1449900]; Youth Innovation Promotion Association of the Chinese Academy of Sciences [2017323]; National Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [DK105562, R01AI132391]; Cancer Research Institute Investigator Award; Pew Charitable Trusts; Burroughs Wellcome FundBurroughs Wellcome Fund; National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [91542102, 31570887, 81571533]; China's Youth 1000-Talent Program; NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Allergy & Infectious Diseases (NIAID) [R01AI132391] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01DK105562] Funding Source: NIH RePORTER
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出版当年[2018]版：
大类 | 1 区 医学
小类 | 1 区 过敏 1 区 免疫学
最新[2023]版：
大类 | 1 区 医学
小类 | 1 区 过敏 1 区 免疫学
JCR分区：
出版当年[2017]版：
Q1 IMMUNOLOGY Q1 ALLERGY
最新[2023]版：
Q1 ALLERGY Q1 IMMUNOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

第一作者：
第一作者机构： [1]Chinese Acad Sci, Shanghai Inst Nutr & Hlth, CAS Key Lab Tissue Microenvironm & Tumor, Univ Chinese Acad Sci,Shanghai Inst Biol Sci, Shanghai, Peoples R China
共同第一作者：
通讯作者：
通讯机构： [1]Chinese Acad Sci, Shanghai Inst Nutr & Hlth, CAS Key Lab Tissue Microenvironm & Tumor, Univ Chinese Acad Sci,Shanghai Inst Biol Sci, Shanghai, Peoples R China [6]Shanghai Jiao Tong Univ, Sch Med, Tongren Hosp, Shanghai 200336, Peoples R China [7]Shanghai Jiao Tong Univ, Sch Med, Shanghai Key Lab Tumor Microenvironm & Inflammat, Shanghai Inst Immunol, Shanghai, Peoples R China [*1]Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, New Lifesciences Building, Rm 1724, No. 320 Yueyang Road, Shanghai 20031, China [*2]Shanghai Jiao Tong University School of Medicine, B5-1202, 280 South Chongqing Road, Shanghai 200025, China [*3]Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
推荐引用方式(GB/T 7714)：
Cai Ting,Qiu Jinxin,Ji Yan,et al.IL-17-producing ST2(+) group 2 innate lymphoid cells play a pathogenic role in lung inflammation[J].JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY.2019,143(1):229-+.doi:10.1016/j.jaci.2018.03.007.
APA：
Cai, Ting,Qiu, Jinxin,Ji, Yan,Li, Wenjing,Ding, Zhaoyun...&Qiu, Ju.(2019).IL-17-producing ST2(+) group 2 innate lymphoid cells play a pathogenic role in lung inflammation.JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY,143,(1)
MLA：
Cai, Ting,et al."IL-17-producing ST2(+) group 2 innate lymphoid cells play a pathogenic role in lung inflammation".JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY 143..1(2019):229-+

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