Journal
CELL REPORTS
Volume 30, Issue 9, Pages 2989-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.02.040
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Funding
- National Institutes of Health/National Heart, Lung, and Blood Institute [R01HL118183, R01HL136586]
- Johns Hopkins 2015 Catalyst Award
- Matthew Vernon Poyner (MVP) Memorial Myocarditis Research Fund
- Myocarditis Foundation 2018 Rhett Lundy Memorial Research Fellowship
- Johns Hopkins Autoimmune Disease Research Center O'Leary-Wilson Fellowship
- Johns Hopkins Bloomberg School of Public Health Richard J. and Margaret Conn Himelfarb Student Support fund
- Katherine E. Welsh Fellowship
- American Heart Association [16POST31330012, 16PRE31170040, 19TPA34910007, 17GRNT33700274]
- American Autoimmune-Related Diseases Association (AARDA)
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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(-/-)II2rg(-/-) 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 Delta dblGATA1 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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