Dissecting mechanisms of innate and acquired immunity in myocarditis

Abstract

Inflammation underlies the pathogenesis of some of the most common cardiovascular diseases. Myocarditis is a relevant clinical cause of heart failure, but also provides an excellent laboratory model to study the mechanisms of inflammation leading to heart failure. The availability of different inbred mouse strains for inducing myocarditis using viral or myosin as triggers provides an excellent platform for investigation. The recent use of genetically manipulated mouse models of transgenic overexpression or knockout or knockin targets have provided opportunity to pinpoint specific pathways underlying myocarditis. These pathways include the involvement of both innate and acquired immunity, as well as the role of viral receptors in disease phenotype. These different models also permit the evaluation of therapeutic strategies of candidates for clinical development.