RNA-binding protein RBM3 intrinsically suppresses lung innate lymphoid cell activation and inflammation partially through CysLT1R

Jana H. Badrani, Allyssa N. Strohm, Lee Lacasa, Blake Civello, Kellen Cavagnero, Yung-An Haung, Michael Amadeo, Luay H. Naji, Sean J. Lund, Anthea Leng, Hyojoung Kim, Rachel E. Baum, Naseem Khorram, Monalisa Mondal, Grégory Seumois, Julie Pilotte, Peter W. Vanderklish, Heather M. McGee and Taylor A. Doherty ()
Additional contact information
Jana H. Badrani: University of California San Diego
Allyssa N. Strohm: University of California San Diego
Lee Lacasa: University of California San Diego
Blake Civello: University of California San Diego
Kellen Cavagnero: University of California San Diego
Yung-An Haung: University of California San Diego
Michael Amadeo: University of California San Diego
Luay H. Naji: University of California San Diego
Sean J. Lund: University of California San Diego
Anthea Leng: University of California San Diego
Hyojoung Kim: University of California San Diego
Rachel E. Baum: University of California San Diego
Naseem Khorram: University of California San Diego
Monalisa Mondal: La Jolla Institute
Grégory Seumois: La Jolla Institute
Julie Pilotte: The Scripps Research Institute
Peter W. Vanderklish: The Scripps Research Institute
Heather M. McGee: University of California San Diego
Taylor A. Doherty: University of California San Diego

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: Abstract Innate lymphoid cells (ILC) promote lung inflammation in asthma through cytokine production. RNA-binding proteins (RBPs) are critical post-transcriptional regulators, although less is known about RBPs in ILC biology. Here, we demonstrate that RNA-binding motif 3 (RBM3) is highly expressed in lung ILCs and is further induced by alarmins TSLP and IL-33. Rbm3−/− and Rbm3−/−Rag2−/− mice exposed to asthma-associated Alternaria allergen develop enhanced eosinophilic lung inflammation and ILC activation. IL-33 stimulation studies in vivo and in vitro show that RBM3 suppressed lung ILC responses. Further, Rbm3−/− ILCs from bone marrow chimeric mice display increased ILC cytokine production suggesting an ILC-intrinsic suppressive function of RBM3. RNA-sequencing of Rbm3−/− lung ILCs demonstrates increased expression of type 2/17 cytokines and cysteinyl leukotriene 1 receptor (CysLT1R). Finally, Rbm3−/−Cyslt1r−/− mice show dependence on CysLT1R for accumulation of ST2+IL-17+ ILCs. Thus, RBM3 intrinsically regulates lung ILCs during allergen-induced type 2 inflammation that is partially dependent on CysLT1R.

Date: 2022
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-022-32176-5 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:13:y:2022:i:1:d:10.1038_s41467-022-32176-5

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

DOI: 10.1038/s41467-022-32176-5

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 ().