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Innate Lymphoid Cells Play a Pathogenic Role in Pericarditis.
- Source :
- Cell Reports; Mar2020, Vol. 30 Issue 9, p2989-2989, 1p
- Publication Year :
- 2020
-
Abstract
- 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 <superscript> −/− </superscript> Il2rg <superscript> −/− </superscript> 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. • ILCs are required for the development of IL-33-induced eosinophilic pericarditis • ILC2s facilitate eotaxin expression in cardiac fibroblasts • Eosinophils in the mediastinum can migrate to the heart during pericarditis • ILCs are more frequently present in the pericardial fluid of pericarditis patients Choi et al. show a pathogenic role for innate lymphoid cells (ILCs) in IL-33-induced eosinophilic pericarditis. ILCs are required for the development of pericarditis, and group 2 ILCs (ILC2s) promote the expression of eotaxin by cardiac fibroblasts. In humans, ILCs are found higher in the pericardial fluid of patients with pericarditis compared to others. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 26391856
- Volume :
- 30
- Issue :
- 9
- Database :
- Complementary Index
- Journal :
- Cell Reports
- Publication Type :
- Academic Journal
- Accession number :
- 142064595
- Full Text :
- https://doi.org/10.1016/j.celrep.2020.02.040