Microbiota-derived peptide mimics drive lethal inflammatory cardiomyopathy

Myocarditis can develop into inflammatory cardiomyopathy through chronic stimulation of myosin heavy chain 6–specific T helper (TH)1 and TH17 cells. However, mechanisms governing the cardiotoxicity programming of heart-specific T cells have remained elusive. Using a mouse model of spontaneous autoimmune myocarditis, we show that progression of myocarditis to lethal heart disease depends on cardiac myosin–specific TH17 cells imprinted in the intestine by a commensal Bacteroides species peptide mimic. Both the successful prevention of lethal disease in mice by antibiotic therapy and the significantly elevated Bacteroides-specific CD4+ T cell and B cell responses observed in human myocarditis patients suggest that mimic peptides from commensal bacteria can promote inflammatory cardiomyopathy in genetically susceptible individuals. The ability to restrain cardiotoxic T cells through manipulation of the microbiome thereby transforms inflammatory cardiomyopathy into a targetable disease.
Source: ScienceNOW - Category: Science Authors: Tags: Immunology, Medicine, Diseases reports Source Type: news

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Source: Current Opinion in Rheumatology - Category: Rheumatology Tags: CLINICAL THERAPEUTICS AND HEMATOLOGIC COMPLICATIONS: Edited by W. Joseph McCune Source Type: research
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