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Myocardial infarction triggers cardioprotective antigen-specific T helper cell responses. 2019
Max Rieckmann, and
Murilo Delgobo, and
Chiara Gaal, and
Lotte Büchner, and
Philipp Steinau, and
Dan Reshef, and
Cristina Gil-Cruz, and
Ellis N Ter Horst, and
Malte Kircher, and
Theresa Reiter, and
Katrin G Heinze, and
Hans Wm Niessen, and
Paul Aj Krijnen, and
Anja M van der Laan, and
Jan J Piek, and
Charlotte Koch, and
Hans-Jürgen Wester, and
Constantin Lapa, and
Wolfgang R Bauer, and
Burkhard Ludewig, and
Nir Friedman, and
Stefan Frantz, and
Ulrich Hofmann, and
Gustavo Campos Ramos
Department of Internal Medicine III, University Clinic Halle, Halle, Germany.
T cell autoreactivity is a hallmark of autoimmune diseases but can also benefit self-maintenance and foster tissue repair. Herein, we investigated whether heart-specific T cells exert salutary or detrimental effects in the context of myocardial infarction (MI), the leading cause of death worldwide. After screening more than 150 class-II-restricted epitopes, we found that myosin heavy chain alpha (MYHCA) was a dominant cardiac antigen triggering post-MI CD4+ T cell activation in mice. Transferred MYHCA614-629-specific CD4+ T (TCR-M) cells selectively accumulated in the myocardium and mediastinal lymph nodes (med-LN) of infarcted mice, acquired a Treg phenotype with a distinct pro-healing gene expression profile, and mediated cardioprotection. Myocardial Treg cells were also detected in autopsies from patients who suffered a MI. Noninvasive PET/CT imaging using a CXCR4 radioligand revealed enlarged med-LNs with increased cellularity in MI-patients. Notably, the med-LN alterations observed in MI patients correlated with the infarct size and cardiac function. Taken together, the results obtained in our study provide evidence showing that MI-context induces pro-healing T cell autoimmunity in mice and confirms the existence of an analogous heart/med-LN/T cell axis in MI patients.
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