ArticleCirculation2013
Alloantibody and complement promote T cell-mediated cardiac allograft vasculopathy through noncanonical nuclear factor-κB signaling in endothelial cells.
Article in Circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 138 citations in OpenAlex.
- Internalized components of membrane attack complexes disrupt proteostasis and acquire alarmin-like properties.Nature communications · 2026Article
- Internalized Components of Membrane Attack Complexes Disrupt Proteostasis and Acquire Alarmin-Like Properties.bioRxiv : the preprint server for biology · 2026Article
- Regulatory T cells in cardiac allograft vasculopathy: from mechanistic insights to clinical tolerance.Frontiers in immunology · 2026Review
- Glycan-encoded immune checkpoints and allorecognition: a mechanistic framework for transplantation and organ engineering.Frontiers in transplantation · 2026Review
- Pathogenesis of Chronic Rejection: Graft Endothelial Cell Trans-presentation of IL-15 Connects Alloantibody- and Cell-Mediated Steps in Allograft Vasculopathy.Results and problems in cell differentiation · 2026Review
- How Cytokines Regulate Immune Response Toward Chronic Allograft Rejection?Results and problems in cell differentiation · 2026Review
- Treatment of antibody-mediated rejection in heart transplantation: from empirical combination to multi-target precision intervention.Frontiers in immunology · 2026Review
- Emerging roles for complement in lung transplantation.The Journal of clinical investigation · 2025Review
- Review
- Maintenance of graft tissue-resident Foxp3+ cells is necessary for lung transplant tolerance in mice.The Journal of clinical investigation · 2025Article
- Role of intrarenal complement production in kidney transplantation.Clinical kidney journal · 2025Review
- Post-transplant Thrombotic Microangiopathy.Journal of the American Society of Nephrology : JASN · 2025Review
- CHIP-ing Away at Post-Transplant Outcomes: the Role of Somatic Mutations in Heart Transplant Outcomes.Journal of cardiac failure · 2025Article
- Identification of a novel biomarker of antibody-mediated rejection in heart transplantation: synergistic effect of anti-nuclear antibodies andFrontiers in immunology · 2025Article
- Loss of Lymphatic IKKα Disrupts Lung Immune Homeostasis, Drives BALT Formation, and Protects against Influenza.ImmunoHorizons · 2024Article
- The transplant rejection response involves neutrophil and macrophage adhesion-mediated trogocytosis and is regulated by NFATc3.Cell death & disease · 2024Article
- Terminal complement complex deposition on chondrocytes promotes premature senescence in age- and trauma-related osteoarthritis.Frontiers in immunology · 2024Article
- In a novel autoimmune and high-pressure glaucoma model a complex immune response is induced.Frontiers in immunology · 2024Article
- Clonal hematopoiesis of indeterminate potential and outcomes after heart transplantation: A multicenter study.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023Article
- A ZFYVE21-Rubicon-RNF34 signaling complex promotes endosome-associated inflammasome activity in endothelial cells.Nature communications · 2023Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCardiac allograft vasculopathy is the major cause of late allograft loss after heart transplantation. Cardiac allograft vasculopathy lesions contain alloreactive T cells that secrete interferon-γ, a vasculopathic cytokine, and occur more frequently in patients with donor-specific antibody. Pathological interactions between these immune effectors, representing cellular and humoral immunity, respectively, remain largely unexplored. METHODS AND
resultsWe used human panel reactive antibody to form membrane attack complexes on allogeneic endothelial cells in vitro and in vivo. Rather than inducing cytolysis, membrane attack complexes upregulated inflammatory genes, enhancing the capacity of endothelial cells to recruit and activate allogeneic interferon-γ--producing CD4(+) T cells in a manner dependent on the activation of noncanonical nuclear factor-κB signaling. Noncanonical nuclear factor-κB signaling was detected in situ within endothelial cells both in renal biopsies from transplantation patients with chronic antibody-mediated rejection and in panel-reactive antibody--treated human coronary artery xenografts in immunodeficient mice. On retransplantation into immunodeficient hosts engrafted with human T cells, panel-reactive antibody--treated grafts recruited more interferon-γ--producing T cells and enhanced cardiac allograft vasculopathy lesion formation.
conclusionsAlloantibody and complement deposition on graft endothelial cells activates noncanonical nuclear factor-κB signaling, initiating a proinflammatory gene program that enhances alloreactive T cell activation and development of cardiac allograft vasculopathy. Noncanonical nuclear factor-κB signaling in endothelial cells, observed in human allograft specimens and implicated in lesion pathogenesis, may represent a target for new pharmacotherapies to halt the progression of cardiac allograft vasculopathy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.