ArticleCirculation research2015
Interferon-γ-mediated allograft rejection exacerbates cardiovascular disease of hyperlipidemic murine transplant recipients.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Prevalence and potential associations of the 2022 newly introduced monocyte value for diagnosis of chronic myelomonocytic leukemia in a general Austrian population.Wiener medizinische Wochenschrift (1946) · 2026Article
- Salivary and Serum Cytokine Concentrations in Kidney Transplantation: A Prospective Study.Oral diseases · 2025Article
- Article
- Th1 cells reduce the osteoblast-like phenotype in valvular interstitial cells by inhibiting NLRP3 inflammasome activation in macrophages.Molecular medicine (Cambridge, Mass.) · 2024Article
- Cellular Heterogeneity of Activated Primary Human Macrophages and Associated Drug-Gene Networks: From Biology to Precision Therapeutics.Circulation · 2023Article
- New insights into maladaptive vascular responses to donor specific HLA antibodies in organ transplantation.Frontiers in transplantation · 2023Review
- Cytokines associated with immune response in atherosclerosis.American journal of translational research · 2022Review
- T cells mediate cell non-autonomous arterial ageing in mice.The Journal of physiology · 2021Article
- The role of interferon-γ in cardiovascular disease: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- IL-27 RαJournal of cellular and molecular medicine · 2020Article
- Innate immune mechanisms in transplant allograft vasculopathy.Current opinion in organ transplantation · 2016Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleTransplantation, the most effective therapy for end-stage organ failure, is markedly limited by early-onset cardiovascular disease (CVD) and premature death of the host. The mechanistic basis of this increased CVD is not fully explained by known risk factors.
objectiveTo investigate the role of alloimmune responses in promoting CVD of organ transplant recipients. METHODS AND
resultsWe established an animal model of graft-exacerbated host CVD by combining murine models of atherosclerosis (apolipoprotein E-deficient recipients on standard diet) and of intra-abdominal graft rejection (heterotopic cardiac transplantation without immunosuppression). CVD was absent in normolipidemic hosts receiving allogeneic grafts and varied in severity among hyperlipidemic grafted hosts according to recipient-donor genetic disparities, most strikingly across an isolated major histocompatibility complex class II antigen barrier. Host disease manifested as increased atherosclerosis of the aorta that also involved the native coronary arteries and new findings of decreased cardiac contractility, ventricular dilatation, and diminished aortic compliance. Exacerbated CVD was accompanied by greater levels of circulating cytokines, especially interferon-γ and other Th1-type cytokines, and showed both systemic and intralesional activation of leukocytes, particularly T-helper cells. Serological neutralization of interferon-γ after allotransplantation prevented graft-related atherosclerosis, cardiomyopathy, and aortic stiffening in the host.
conclusionsOur study reveals that sustained activation of the immune system because of chronic allorecognition exacerbates the atherogenic diathesis of hyperlipidemia and results in de novo cardiovascular dysfunction in organ transplant recipients.
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