Asset Details
Do you wish to reserve the book?
Microbiota-derived peptide mimics drive lethal inflammatory cardiomyopathy
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Microbiota-derived peptide mimics drive lethal inflammatory cardiomyopathy
Do you wish to request the book?
Microbiota-derived peptide mimics drive lethal inflammatory cardiomyopathy
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Microbiota-derived peptide mimics drive lethal inflammatory cardiomyopathy
2019
Overview
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.
Publisher
American Association for the Advancement of Science,The American Association for the Advancement of Science
Subject
/ Antigens
/ Autoimmune Diseases - complications
/ Autoimmune Diseases - immunology
/ beta-Galactosidase - immunology
/ Cardiomyopathy, Dilated - immunology
/ Cardiomyopathy, Dilated - microbiology
/ CD4-Positive T-Lymphocytes - immunology
/ Chains
/ Gastrointestinal Microbiome - immunology
/ Heart
/ Humans
/ Mice
/ Mimicry
/ Muscles
/ Myosin
/ Myosin Heavy Chains - genetics
/ Myosin Heavy Chains - immunology
/ Peptides
