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- W4313305885 abstract "Abstract Myocarditis is the inflammation of the cardiac muscle and is among the leading causes of sudden cardiac failure in young adults. We demonstrate here that natural killer (NK) cells, a subset of the Type I innate lymphoid cell (ILC) group, suppress experimental autoimmune myocarditis (EAM). EAM was initiated in BALB/c mice by immunization with myocarditogenic peptide emulsified in complete Freund's adjuvant. During disease, activated cardiac NK cells accumulated in the heart, secreted interferonγ, perforin, and granzyme-B, and expressed activation markers CD69, TRAIL, and CD27. The depletion of NK cells during EAM with anti-asialo GM1 antibody resulted in a 10-fold increase from 0.12 - 12.0% in the percentage of eosinophils found in the cardiac tissue at the peak of disease. This was accompanied by significantly increased myocarditis severity and elevated fibrosis. Eosinophils were required for the change in disease severity in the absence of NK cells, as treatment with anti-asialo GM1 did not increase myocarditis severity in eosinophil-deficient ΔdoubleGATA1 mice. We show that NK cells limited eosinophilic infiltration during EAM indirectly through altering eosinophil-related chemokine production by resident cardiac fibroblasts both in vitro and in vivo. Additionally, the co-culture of NK cells and eosinophils directly induced eosinophil apoptosis in vitro. Altogether, we define a new pathway of eosinophilic regulation through interactions with NK cells." @default.
- W4313305885 created "2023-01-06" @default.
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- W4313305885 date "2015-05-01" @default.
- W4313305885 modified "2023-09-25" @default.
- W4313305885 title "Natural killer cells protect against cardiac inflammation and fibrosis by directly limiting eosinophilic accumulation (BA7P.144)" @default.
- W4313305885 doi "https://doi.org/10.4049/jimmunol.194.supp.115.4" @default.
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