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Published on: January 23, 2019
Peripheral expansion of circulating T-helper 1 cells predicts coronary endothelial dysfunction after cardiac
Heiko Methe1, Daniela Wiegand, Ulrich Welsch
1Department of Cardiology, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany. heiko.methe@med.uni-muenchen.de
Insights
Peripheral expansion of T-helper 1 (Th1) cells indicates endothelial dysfunction after heart transplantation. Monitoring Th1 cells may help predict transplant vasculopathy development in cardiac transplant recipients.
Area of Science:
- Immunology
- Cardiology
- Transplantation Science
Background:
- Chronic rejection remains a major cause of death after heart transplantation.
- Transplant vasculopathy, a form of arteriosclerosis, characterizes chronic rejection.
- The precise mechanisms driving transplant vasculopathy are not fully understood.
Purpose of the Study:
- To investigate the role of T-helper 1 (Th1) cells in the development of cardiac allograft vasculopathy.
- To assess the correlation between T-cell subsets and early indicators of transplant vasculopathy.
Main Methods:
- Characterized T-cell subsets in 32 heart transplant recipients using RT-PCR, flow cytometry, and immunohistochemistry.
- Assessed endothelial function via coronary flow reserve testing.
- Correlated T-cell findings with endothelial function test results.
Main Results:
- Patients with allograft endothelial dysfunction showed significantly higher mRNA levels of Th1 cytokines (interferon-gamma, interleukin-2) and STAT4.
- A significant increase in circulating CD3+/interferon-gamma+ T-cells was observed in patients with endothelial dysfunction.
- No significant differences in Th2 cytokine or STAT6 levels were found between groups.
Conclusions:
- Peripheral expansion of Th1 cells, but not Th2 cells, predicts coronary endothelial dysfunction post-cardiac transplantation.
- Quantifying circulating T-cells could serve as a diagnostic tool for predicting endothelial dysfunction in heart transplant patients.
Objective:
We sought to assess the importance of Th1 cells for the development of cardiac allograft vasculopathy.
Background:
Despite improvements in immunosuppressive regimens, chronic rejection still represents one of the leading causes of death beyond the first year after heart transplantation. Chronic rejection is characterized by the development of transplant vasculopathy. The exact mechanisms initiating and promoting this form of arteriosclerosis in the human setting remain unclear.
Methods:
In order to assess the role of T lymphocytes we characterized differentiated T-cell subsets in 32 transplant recipients early after transplantation using RT-PCR, flow cytometry and immunhistochemistry and matched these findings with endothelial function testing as an early clinical indicator of transplant vasculopathy.
Results:
Allograft endothelial dysfunction (ED) was defined as a compromised coronary flow reserve to acetylcholine (CFVR<2 in 8 of 32 transplant recipients). In these patients, mRNA transcript levels for the T-helper (Th)1 signature cytokines interferon (INF)-gamma (p<0.0001) and interleukin (IL)-2 (p<0.005) and STAT4 (Th1 transcription factor, p<0,05) were significantly higher than in the remaining 24 patients with normal endothelial function. This correlated with a significant increase in circulating CD3(+)/IFN-gamma(+)-T-cells (28.6 +/- 4.4% vs 8.7 +/- 5.6%; p<0.0001). In contrast, transcript levels for the Th2 signature cytokines (IL-4, IL-10) and STAT6 (Th2 transcription factor) did not differ significantly between the two groups.
Conclusions:
Peripheral expansion of circulating Th1 but not Th2 cells predicts coronary ED after cardiac transplantation. Therefore, quantification of circulating T cells might be a diagnostic tool to predict development of ED in patients after heart transplantation.
