ArticleAtherosclerosis2012
Inflammatory Ly-6C(hi) monocytes play an important role in the development of severe transplant arteriosclerosis in hyperlipidemic recipients.
Article in Atherosclerosis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Anti?atherosclerotic effect of aged garlic extract: Mode of action and therapeutic benefits (Review).Experimental and therapeutic medicine · 2025Review
- Mapping Transplant Arteriosclerosis Cell-by-Cell: A Path to New Immune Insights.Circulation research · 2020Article
- Genome-wide non-HLA donor-recipient genetic differences influence renal allograft survival via early allograft fibrosis.Kidney international · 2020Article
- Acute and chronic phagocyte determinants of cardiac allograft vasculopathy.Seminars in immunopathology · 2018Review
- Decreased circulating and neutrophil mediated VEGF-A165 release in stable long-term cardiac transplant recipients.Vascular cell · 2015Article
- Continuous retinoic acid induces the differentiation of mature regulatory monocytes but fails to induce regulatory dendritic cells.BMC immunology · 2014Article
- Therapeutic inflammatory monocyte modulation using immune-modifying microparticles.Science translational medicine · 2014Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
objectiveTransplant arteriosclerosis (TA) restricts long-term survival of heart transplant recipients. Although the role of monocyte/macrophages is well established in native atherosclerosis, it has been studied to a much lesser extent in TA. Plasma cholesterol is the most important non-immunologic risk factor for development of TA but the underlying mechanisms are largely unknown. We hypothesized that monocyte/macrophages might play an important role in the pathogenesis of TA under hyperlipidemic conditions.
methodsWe studied TA in fully mismatched arterial allografts transplanted into hyperlipidemic ApoE(-/-) recipients compared to wild-type controls. The recruitment of distinct monocyte populations into the grafts was tracked by in vivo labelling with fluorescent microspheres. We used antibody-mediated depletion protocols to dissect the relative contribution of T lymphocytes and monocytes to disease development.
resultsIn the hyperlipidemic environment the progression of TA was highly exacerbated and the inflammatory CD11b(+)CD115(+)Ly-6C(hi) monocytes were preferentially recruited into the neointima. The number of macrophage-derived foam cells present in the grafts strongly correlated with plasma cholesterol and disease severity. Depletion of Ly-6C(hi) monocytes and neutrophils significantly inhibited macrophage accumulation and disease progression. The accelerated monocyte recruitment occurs through a T cell-independent mechanism, as T cell depletion did not influence macrophage accumulation into the grafts.
conclusionsOur study identifies for the first time the involvement of inflammatory Ly-6C(hi) monocytes into the pathogenesis of TA, particularly in conditions of hyperlipidemia. Targeted therapies modulating the recruitment and activation of these cells could potentially delay coronary allograft vasculopathy and improve long-term survival of heart transplant recipients.
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