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Gil-Cruz, Cristina; Perez-Shibayama, Christian; De Martin, Angelina; Ronchi, Francesca; van der Borght, Katrien; Niederer, Rebekka; Onder, Lucas; Lütge, Mechthild; Novkovic, Mario; Nindl, Veronika; Ramos, Gustavo; Arnoldini, Markus; Slack, Emma M C; Boivin-Jahns, Valérie; Jahns, Roland; Wyss, Madeleine; Mooser, Catherine; Lambrecht, Bart N; Maeder, Micha T; Rickli, Hans; Flatz, Lukas; Eriksson, Urs; Geuking, Markus B; McCoy, Kathy D; Ludewig, Burkhard
Science (American Association for the Advancement of Science), 11/2019, Letnik: 366, Številka: 6467Journal Article
Myocarditis can develop into inflammatory cardiomyopathy through chronic stimulation of myosin heavy chain 6-specific T helper (T )1 and T 17 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 T 17 cells imprinted in the intestine by a commensal species peptide mimic. Both the successful prevention of lethal disease in mice by antibiotic therapy and the significantly elevated 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.
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in: SICRIS
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