{'fraction_non_alphanumeric': 0.018094089264173704, 'fraction_numerical': 0.0036188178528347406, 'mean_word_length': 5.859504132231405, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Elution of autoantibodies from the hearts of coxsackievirus-infected mice.

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.