Innate Lymphoid Cells Play a Pathogenic Role in Pericarditis
Open accessAbstract
We find that cardiac group 2 innate lymphoid cells (ILC2s) are essential for the development of IL-33-induced eosinophilic pericarditis. We show a pathogenic role for ILC2s in cardiac inflammation, in which ILC2s activated by IL-33 drive the development of eosinophilic pericarditis in collaboration with cardiac fibroblasts. ILCs, not T and B cells, are required for the development of pericarditis. ILC2s transferred to the heart of Rag2 −/− Il2rg −/− mice restore their susceptibility to eosinophil infiltration. Moreover, ILC2s direct cardiac fibroblasts to produce eotaxin-1. We also find that eosinophils reside in the mediastinal cavity and that eosinophils transferred to the mediastinal cavity of eosinophil-deficient ΔdblGATA1 mice following IL-33 treatment migrate to the heart. Thus, the serous cavities may serve as a reservoir of cardiac-infiltrating eosinophils. In humans, patients with pericarditis show higher amounts of ILCs in pericardial fluid than do healthy controls and patients with other cardiac diseases. We demonstrate that ILCs play a critical role in pericarditis.
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Autoantibodies against α-MyHC are detected in mice with eosinophilic myopericarditis induced by recombinant IL-33 administration.
“autoantibodies against α -MyHC have been detected in mice with eosinophilic myopericarditis, which involves inflamed myocardium and pericardium, induced by recombinant IL-33 in vivo administration.”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [208]
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- Authors
- Choi, H. S., Won, T., Hou, X., Chen, G., Bracamonte-Baran, W., Talor, M. V., Jurčová, I., Szárszoi, O., Čurnova, L., Stříž, I., Hooper, J. E., Melenovský, V., & Čiháková, D.
- Affiliations
- Johns Hopkins University (US)
- Institute of Clinical and Experimental Medicine (CZ)
- Corresponding author
- Čiháková, Daniela
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2020-03
- Volume
- 30
- Issue
- 9
- Pages
- 2989-3003.e6
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC7332109
- OpenAlex
- W3009586792
- Cited by
- 43
- References
- 74
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 6 · 2023: 6 · 2022: 8 · 2021: 7 · 2020: 4
- FWCI
- 2.19
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Mayo Clinic
- American Heart Association (16PRE31170040, 17GRNT33700274, 19TPA34910007)
- American Autoimmune Related Diseases Association
- Johns Hopkins University
- Myocarditis Foundation
- National Heart, Lung, and Blood Institute (R01HL118183, R01HL136586)
- National Institutes of Health
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Pericarditis and Cardiac Tamponade
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- innate lymphoid cells, ILC2, IL-33, eosinophils, cardiac fibroblasts, eotaxin, cardiac inflammation, pericardial fluid
- MeSH terms
- Interleukin-33, Interleukin-1 Receptor-Like 1 Protein, Animals, Cell Movement, Disease Susceptibility, Eosinophils, Female, Fibroblasts, Gene Expression Regulation, Heart, Heart Function Tests, Humans, Immunity, Innate, Lymphocytes, Male, Mediastinum, Mice, Inbred BALB C, Pericarditis, Signal Transduction, Interleukin-5, Up-Regulation, Chemokine CCL11
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