Key result
Heart-reactive antibodies were successfully eluted from the hearts of Coxsackievirus B3-infected A/J mice with autoimmune myocarditis, but not from resistant B10.A mice.
This study provides direct evidence that heart-reactive autoantibodies bind to cardiac tissue in susceptible mice following Coxsackievirus infection, supporting their potential pathogenic role in chronic myocarditis.
Tissue-bound heart-reactive autoantibodies occur in susceptible myocarditis models; leaves open their pathogenic role and therapeutic targeting in human disease.
Circulating heart-reactive antibodies are commonly reported in myocarditis and cardiomyopathy patients. While these observations support the hypothesis that autoimmune mechanisms may be involved in pathogenesis, such evidence is largely circumstantial. The current studies demonstrate that heart-reactive antibodies can be eluted from the hearts of infected Coxsackievirus B3-infected A/J mice with post-infectious autoimmune myocarditis, but not from the hearts of infected B10.A mice which are resistant to autoimmune myocarditis. The eluted antibodies recognize fewer cardiac antigens than are recognized by circulating antibodies. These results provide an opportunity to examine the role of autoantibodies in the pathogenesis of chronic myocarditis.
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Neumann et al. (1991) studied Post-infectious autoimmune myocarditis. Coxsackievirus B3 infection in A/J mice vs. Coxsackievirus B3 infection in B10.A mice was evaluated on Elution of heart-reactive antibodies. Heart-reactive antibodies were successfully eluted from the hearts of Coxsackievirus B3-infected A/J mice with autoimmune myocarditis, but not from resistant B10.A mice.
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