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.
- MeSH
- Chemokine CCL11 genetics metabolism MeSH
- Eosinophils drug effects pathology MeSH
- Fibroblasts drug effects metabolism MeSH
- Heart Function Tests drug effects MeSH
- Interleukin-33 pharmacology MeSH
- Interleukin-1 Receptor-Like 1 Protein deficiency metabolism MeSH
- Interleukin-5 metabolism MeSH
- Humans MeSH
- Lymphocytes drug effects immunology MeSH
- Mediastinum pathology MeSH
- Mice, Inbred BALB C MeSH
- Disease Susceptibility MeSH
- Pericarditis genetics immunology physiopathology MeSH
- Cell Movement drug effects MeSH
- Immunity, Innate * drug effects MeSH
- Gene Expression Regulation drug effects MeSH
- Signal Transduction drug effects MeSH
- Heart drug effects physiopathology MeSH
- Up-Regulation drug effects MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
