Publikation

Microbiota-derived peptide mimics drive lethal inflammatory cardiomyopathy

Wissenschaftlicher Artikel/Review - 15.11.2019

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Link to Abstract: http://science.sciencemag.org/cgi/content/abstract/366/6467/881?ijkey=prWyn9fm3ctEE&keytype=ref&siteid=sci

Link to Reprint: http://science.sciencemag.org/cgi/rapidpdf/366/6467/881?ijkey=prWyn9fm3ctEE&keytype=ref&siteid=sci
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Zitation
Gil Cruz C, Jahns R, Wyss M, Mooser C, Lambrecht B, Maeder M, Rickli H, Flatz L, Eriksson U, Geuking M, McCoy K, Boivin-Jahns V, Slack E, Arnoldini M, Pérez Shibayama C, De Martin A, Ronchi F, Van der Borght K, Niederer R, Onder L, Lütge M, Novkovic M, Nindl V, Ramos G, Ludewig B. Microbiota-derived peptide mimics drive lethal inflammatory cardiomyopathy. Science 2019; 366:881-886.
Art
Wissenschaftlicher Artikel/Review (Englisch)
Zeitschrift
Science 2019; 366
Veröffentlichungsdatum
15.11.2019
eISSN (Online)
1095-9203
Seiten
881-886
Kurzbeschreibung/Zielsetzung

Myocarditis can develop into inflammatory cardiomyopathy through chronic stimulation of myosin heavy chain 6-specific T helper (T)1 and T17 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 T17 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.