The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation
IL-33 orchestrates type 2 immunity in allergic asthma. Here the authors show, using biochemical, structural and patient data, that upon IL-33 or allergic challenge, the isomerase Pin1 modifies IRAK-M to control the production of pro-inflammatory cytokines in the setting of airway inflammation.
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2018-04-01
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Online Access: | https://doi.org/10.1038/s41467-018-03886-6 |
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doaj-f59a26dd71a44b3c90785a69ce33bbf82021-05-11T10:09:44ZengNature Publishing GroupNature Communications2041-17232018-04-019111910.1038/s41467-018-03886-6The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammationMorris Nechama0Jeahoo Kwon1Shuo Wei2Adrian Tun Kyi3Robert S. Welner4Iddo Z. Ben-Dov5Mohamed S. Arredouani6John M. Asara7Chun-Hau Chen8Cheng-Yu Tsai9Kyle F. Nelson10Koichi S Kobayashi11Elliot Israel12Xiao Zhen Zhou13Linda K. Nicholson14Kun Ping Lu15Division of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDepartment of Molecular Biology & Genetics, Cornell UniversityDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDepartment of Nephrology and Hypertension, Hadassah-Hebrew Medical CenterDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDepartment of Medicine, Brigham and Women’s HospitalDepartment of Microbial Pathogenesis & Immunology, Texas A&M Health Science Center, College StationDepartment of Medicine, Brigham and Women’s HospitalDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolDepartment of Molecular Biology & Genetics, Cornell UniversityDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical SchoolIL-33 orchestrates type 2 immunity in allergic asthma. Here the authors show, using biochemical, structural and patient data, that upon IL-33 or allergic challenge, the isomerase Pin1 modifies IRAK-M to control the production of pro-inflammatory cytokines in the setting of airway inflammation.https://doi.org/10.1038/s41467-018-03886-6 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Morris Nechama Jeahoo Kwon Shuo Wei Adrian Tun Kyi Robert S. Welner Iddo Z. Ben-Dov Mohamed S. Arredouani John M. Asara Chun-Hau Chen Cheng-Yu Tsai Kyle F. Nelson Koichi S Kobayashi Elliot Israel Xiao Zhen Zhou Linda K. Nicholson Kun Ping Lu |
spellingShingle |
Morris Nechama Jeahoo Kwon Shuo Wei Adrian Tun Kyi Robert S. Welner Iddo Z. Ben-Dov Mohamed S. Arredouani John M. Asara Chun-Hau Chen Cheng-Yu Tsai Kyle F. Nelson Koichi S Kobayashi Elliot Israel Xiao Zhen Zhou Linda K. Nicholson Kun Ping Lu The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation Nature Communications |
author_facet |
Morris Nechama Jeahoo Kwon Shuo Wei Adrian Tun Kyi Robert S. Welner Iddo Z. Ben-Dov Mohamed S. Arredouani John M. Asara Chun-Hau Chen Cheng-Yu Tsai Kyle F. Nelson Koichi S Kobayashi Elliot Israel Xiao Zhen Zhou Linda K. Nicholson Kun Ping Lu |
author_sort |
Morris Nechama |
title |
The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation |
title_short |
The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation |
title_full |
The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation |
title_fullStr |
The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation |
title_full_unstemmed |
The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation |
title_sort |
il-33-pin1-irak-m axis is critical for type 2 immunity in il-33-induced allergic airway inflammation |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2018-04-01 |
description |
IL-33 orchestrates type 2 immunity in allergic asthma. Here the authors show, using biochemical, structural and patient data, that upon IL-33 or allergic challenge, the isomerase Pin1 modifies IRAK-M to control the production of pro-inflammatory cytokines in the setting of airway inflammation. |
url |
https://doi.org/10.1038/s41467-018-03886-6 |
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