The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation

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 () and Kun Ping Lu ()
Additional contact information
Morris Nechama: Beth Israel Deaconess Medical Center, Harvard Medical School
Jeahoo Kwon: Cornell University
Shuo Wei: Beth Israel Deaconess Medical Center, Harvard Medical School
Adrian Tun-Kyi: Beth Israel Deaconess Medical Center, Harvard Medical School
Robert S. Welner: Beth Israel Deaconess Medical Center, Harvard Medical School
Iddo Z. Ben-Dov: Hadassah-Hebrew Medical Center
Mohamed S. Arredouani: Beth Israel Deaconess Medical Center, Harvard Medical School
John M. Asara: Beth Israel Deaconess Medical Center, Harvard Medical School
Chun-Hau Chen: Beth Israel Deaconess Medical Center, Harvard Medical School
Cheng-Yu Tsai: Beth Israel Deaconess Medical Center, Harvard Medical School
Kyle F. Nelson: Brigham and Women’s Hospital
Koichi S Kobayashi: Department of Microbial Pathogenesis & Immunology, Texas A&M Health Science Center, College Station
Elliot Israel: Brigham and Women’s Hospital
Xiao Zhen Zhou: Beth Israel Deaconess Medical Center, Harvard Medical School
Linda K. Nicholson: Cornell University
Kun Ping Lu: Beth Israel Deaconess Medical Center, Harvard Medical School

Nature Communications, 2018, vol. 9, issue 1, 1-19

Abstract: Abstract Interleukin 33 (IL-33) is among the earliest-released cytokines in response to allergens that orchestrate type 2 immunity. The prolyl cis-trans isomerase PIN1 is known to induce cytokines for eosinophil survival and activation by stabilizing cytokines mRNAs, but the function of PIN1 in upstream signaling pathways in asthma is unknown. Here we show that interleukin receptor associated kinase M (IRAK-M) is a PIN1 target critical for IL-33 signaling in allergic asthma. NMR analysis and docking simulations suggest that PIN1 might regulate IRAK-M conformation and function in IL-33 signaling. Upon IL-33-induced airway inflammation, PIN1 is activated for binding with and isomerization of IRAK-M, resulting in IRAK-M nuclear translocation and induction of selected proinflammatory genes in dendritic cells. Thus, the IL-33-PIN1-IRAK-M is an axis critical for dendritic cell activation, type 2 immunity and IL-33 induced airway inflammation.

Date: 2018
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-018-03886-6 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03886-6

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-018-03886-6

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().