Evaluation of cardiac autoantibodies during acute cellular heart transplant rejection

Christian Salbach (Heidelberg)1, P. Schlegel (Heidelberg)1, V. Stroikova (Heidelberg)1, M. Helmschrott (Heidelberg)1, A.-M. Müller (Heidelberg)1, C. Weiß (Mannheim)2, E. Giannitsis (Heidelberg)1, N. Frey (Heidelberg)1, Z. Kaya (Heidelberg)1

1Universitätsklinikum Heidelberg Klinik für Innere Med. III, Kardiologie, Angiologie u. Pneumologie Heidelberg, Deutschland; 2Institut für Medizinische Statistik, Biomathematik und Informationsverarbeitung Mannheim, Deutschland


Background. Acute cellular heart transplant rejection (ACR) is thought to be accompanied by cardiac cell death leading to an exposure of former unknown cardiac autoantigens to the host immune system.  Therefore, heat transplanted (HTx) individuals developing an ACR might produce cardiac autoantibodies (aABs) in response to heat transplant rejection. This study aimed to evaluate the evidence of cardiac aABs in HTx individuals during ACR utilizing a peptide-array approach.

Methods. In this retrospective single-center study 37 HTx patients developing an ACR at the University Hospital of Heidelberg were included. Cardiac magnetic resonance imaging proven healthy age- and gender matched individuals were chosen as control. Sera from HTx patients were obtained during endomyocardial biopsy and screened for 130 partially overlapping cardiac aABs using a peptide-array approach. Peptide sequences for the array were chosen after comprehensive literature search for immunogenic peptide sequences known to be associated with heart failure, dilated cardiomyopathy, and myocarditis in animal or human.

Results. HTx patients showed suppressed cardiac aABs in comparison to healthy individuals. However, cardiac aABs corresponding to a sequence of troponin I (TnI) were significantly upregulated in HTx patients without ACR compared to healthy individuals. Additionally, a comparison between cardiac aABs during ACR revealed aABs against the peptide sequence of beta-2-adrenergic receptor to be upregulated during ACR, whereas aABs against the peptide sequence of TnI were downregulated during ACR.

Conclusion. Within this study, we could show the feasibility of using a peptide-array approach as a screening tool for cardiac aABs against structural peptides in post HTx patients. Furthermore, we could identify two differentially regulated cardiac aABs during ACR in post HTx patients. However, this study was designed as a feasibility analysis and further studies are needed to evaluate the role of cardiac aABs during ACR.

Funding This work was supported by the German Research Foundation and the Else-Fresenius Stiftung.


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