Key result
Myosin-induced autoimmune myocarditis can be induced in susceptible mice and Lewis rats by immunization with purified cardiac myosin or adoptive transfer of myosin-reactive T cells, peaking at 21 days.
This paper outlines established protocols for inducing experimental autoimmune myocarditis in mice and rats to study immune-mediated cardiac damage.
Facilitates preclinical investigation of immune-mediated myocarditis; leaves open translation to human disease and therapies.
Myosin-induced autoimmune myocarditis (EAM) is a model of inflammatory heart disease initiated by CD4(+) T cells. It is a paradigm of the immune-mediated cardiac damage believed to play a role in the pathogenesis of a subset of postinfectious human cardiomyopathies. Myocarditis is induced in susceptible mice by immunization with purified cardiac myosin or specific peptides derived from cardiac myosin, or by adoptive transfer of myosin-reactive T cells. Myocarditis is induced in Lewis rats by immunization with purified cardiac myosin or by adoptive transfer of T cells stimulated by specific peptides derived from cardiac myosin. Myocarditis begins 12 to 14 days after the first immunization, and is maximal after 21 days. In addition to the protocols used to induce EAM in mice and rats, support protocols are included for preparing purified cardiac myosin using mouse or rat heart tissue, preparing purified cardiac myosin for injection, and collecting and assessing hearts by histopathological means.
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Stacy C. Smith (1999) conducted a review in Autoimmune Myocarditis. Immunization with purified cardiac myosin or adoptive transfer of myosin-reactive T cells was evaluated on Myocarditis induction. Myosin-induced autoimmune myocarditis can be induced in susceptible mice and Lewis rats by immunization with purified cardiac myosin or adoptive transfer of myosin-reactive T cells, peaking at 21 days.
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