Key result
Eosinophil deficiency or eosinophil-specific IL-4 deletion protected mice from progressing from experimental autoimmune myocarditis to inflammatory dilated cardiomyopathy.
Why the study?
Does eosinophil-derived IL-4 drive the progression of experimental autoimmune myocarditis to inflammatory dilated cardiomyopathy?
Population
Experimental autoimmune myocarditis mouse models including WT, eosinophil-deficient ΔdblGATA1…
Comparison
Genetic deletion or overexpression of… vs Wild-type (WT) mice or respective genetic controls
Design
Preclinical
Authors
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Supports eosinophil IL-4 targeting in murine myocarditis models; leaves open translation to human inflammatory dilated cardiomyopathy.
Does eosinophil-derived IL-4 drive the progression of experimental autoimmune myocarditis to inflammatory dilated cardiomyopathy?
Eosinophils drive the progression of myocarditis to inflammatory dilated cardiomyopathy through the production of IL-4 in a mouse model.
Diny et al. (2017) studied Myocarditis and inflammatory dilated cardiomyopathy. Eosinophil deficiency or eosinophil-specific IL-4 deletion vs. Wild-type mice was evaluated on Progression to inflammatory dilated cardiomyopathy and heart failure. Eosinophil deficiency or eosinophil-specific IL-4 deletion protected mice from progressing from experimental autoimmune myocarditis to inflammatory dilated cardiomyopathy.
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