T cell–intrinsic ASC critically promotes TH17-mediated experimental autoimmune encephalomyelitis

被引:0
|
作者
Bradley N Martin
Chenhui Wang
Cun-jin Zhang
Zizhen Kang
Muhammet Fatih Gulen
Jarod A Zepp
Junjie Zhao
Guanglin Bian
Jeong-su Do
Booki Min
Paul G Pavicic
Caroline El-Sanadi
Paul L Fox
Aoi Akitsu
Yoichiro Iwakura
Anasuya Sarkar
Mark D Wewers
William J Kaiser
Edward S Mocarski
Marc E Rothenberg
Amy G Hise
George R Dubyak
Richard M Ransohoff
Xiaoxia Li
机构
[1] Cleveland Clinic Lerner Research Institute,Department of Immunology
[2] Case Western Reserve University School of Medicine,Department of Pathology
[3] Key Laboratory of Molecular Biophysics of the Ministry of Education,Department of Neurology
[4] College of Life Science and Technology,Department of Immunology
[5] Huazhong University of Science and Technology,Department of Physiology and Biophysics
[6] Tianjin Neurological Institute,Department of Cellular and Molecular Medicine
[7] Tianjin Medical University General Hospital,Department of Microbiology and Immunology
[8] Tianjin Neurological Institute,Division of Allergy and Immunology
[9] Tianjin Medical University General Hospital,Department of Neurosciences
[10] Shanghai Institute of Immunology,undefined
[11] Shanghai Jiaotong University School of Medicine,undefined
[12] Case Western Reserve University School of Medicine,undefined
[13] Cleveland Clinic Lerner Research Institute,undefined
[14] Research Institute for Biomedical Sciences,undefined
[15] Tokyo University of Science,undefined
[16] Yamazaki,undefined
[17] Davis Heart and Lung Research Institute,undefined
[18] Ohio State University College of Medicine,undefined
[19] Emory Vaccine Center,undefined
[20] Cincinnati Children's Hospital Medical Center,undefined
[21] Center for Global Health and Diseases,undefined
[22] Case Western Reserve University,undefined
[23] Cleveland Clinic Lerner Research Institute,undefined
[24] Present address: Biogen Idec,undefined
[25] Cambridge,undefined
[26] Massachusetts,undefined
[27] USA.,undefined
来源
Nature Immunology | 2016年 / 17卷
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摘要
Inflammasome activation triggers the release of active interleukin 1β (IL-1β). Li and colleagues show that TH17 cells can release IL-1β upon T cell antigen receptor and ATP stimulation via an ASC–NLPR3–caspase-8 axis, thereby contributing to neuroinflammation.
引用
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页码:583 / 592
页数:9
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