T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure
2017 | journal article; research paper
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T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure
Gröschel, C. ; Sasse, A. ; Röhrborn, C. ; Monecke, S. ; Didié, M. ; Elsner, L. & Kruse, V. et al. (2017)
Scientific Reports, 7(1) art. 15998. DOI: https://doi.org/10.1038/s41598-017-16147-1
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Details
- Authors
- Gröschel, Carina ; Sasse, André ; Röhrborn, Charlotte ; Monecke, Sebastian ; Didié, Michael ; Elsner, Leslie ; Kruse, Vanessa ; Bunt, Gertrude; Lichtman, Andrew H.; Toischer, Karl ; Zimmermann, Wolfram-Hubertus ; Dressel, Ralf ; Hasenfuß, Gerd
- Abstract
- We investigated whether CD4+-T cells with specificity for an antigen in cardiomyocytes promote the progression from hypertrophy to heart failure in mice with increased pressure load due to transverse aortic constriction (TAC). OT-II mice expressing a transgenic T cell receptor (TCR) with specificity for ovalbumin (OVA) on CD4+-T cells and cMy-mOVA mice expressing OVA on cardiomyocytes were crossed. The resulting cMy-mOVA-OT-II mice did not display signs of spontaneous autoimmunity despite the fact that their OVA-specific CD4+-T cells were not anergic. After TAC, progression to heart failure was significantly accelerated in cMy-mOVA-OT-II compared to cMy-mOVA mice. No OVA-specific antibodies were induced in response to TAC in cMy-mOVA-OT-II mice, yet more CD3+ T cells infiltrated their myocardium when compared with TAC-operated cMy-mOVA mice. Systemically, the proportion of activated CD4+-T cells with a Th1 and Th17 cytokine profile was increased in cMy-mOVA-OT-II mice after TAC. Thus, T helper cells with specificity for an antigen in cardiomyocytes can directly promote the progression of heart failure in response to pressure overload independently of autoantibodies.
- Issue Date
- 2017
- Journal
- Scientific Reports
- Project
- SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz
SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur
SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien
SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation
SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle - Working Group
- RG Dressel
RG Hasenfuß (Transition zur Herzinsuffizienz)
RG Toischer (Kardiales Remodeling)
RG Zimmermann (Engineered Human Myocardium) - ISSN
- 2045-2322
- Language
- English
- Sponsor
- Open-Access-Publikationsfonds 2017