作者: Hee Sun Choi , Taejoon Won , Xuezhou Hou , Guobao Chen , William Bracamonte-Baran
DOI: 10.1016/J.CELREP.2020.02.040
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摘要: Summary We find that cardiac group 2 innate lymphoid cells (ILC2s) are essential for the development of IL-33-induced eosinophilic pericarditis. show a pathogenic role ILC2s in inflammation, which activated by IL-33 drive pericarditis collaboration with fibroblasts. ILCs, not T and B cells, required transferred to heart Rag2−/−Il2rg−/− mice restore their susceptibility eosinophil infiltration. Moreover, direct fibroblasts produce eotaxin-1. also eosinophils reside mediastinal cavity eosinophil-deficient ΔdblGATA1 following treatment migrate heart. Thus, serous cavities may serve as reservoir cardiac-infiltrating eosinophils. In humans, patients higher amounts ILCs pericardial fluid than do healthy controls other diseases. demonstrate play critical