ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2016
Complement C5 Inhibition Reduces T Cell-Mediated Allograft Vasculopathy Caused by Both Alloantibody and Ischemia Reperfusion Injury in Humanized Mice.
Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- A ZFYVE21-Rubicon-RNF34 signaling complex promotes endosome-associated inflammasome activity in endothelial cells.Nature communications · 2023Article
- Hedgehog-induced ZFYVE21 promotes chronic vascular inflammation by activating NLRP3 inflammasomes in T cells.Science signaling · 2023Article
- Hedgehog costimulation during ischemia-reperfusion injury potentiates cytokine and homing responses of CD4Frontiers in immunology · 2023Article
- Monobody adapter for functional antibody display on nanoparticles for adaptable targeted delivery applications.Nature communications · 2022Article
- Membrane attack complexes, endothelial cell activation, and direct allorecognition.Frontiers in immunology · 2022Review
- Beyond Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome: The Relevance of Complement From Pathogenesis to Pregnancy Outcome in Other Systemic Rheumatologic Diseases.Frontiers in pharmacology · 2022Review
- Cardiac allograft vasculopathy: current review and future research directions.Cardiovascular research · 2021Review
- The Endothelial Glycocalyx as a Target of Ischemia and Reperfusion Injury in Kidney Transplantation-Where Have We Gone So Far?International journal of molecular sciences · 2021Review
- Complement-activated interferon-γ-primed human endothelium transpresents interleukin-15 to CD8+ T cells.The Journal of clinical investigation · 2020Article
- Complement Membrane Attack Complex: New Roles, Mechanisms of Action, and Therapeutic Targets.The American journal of pathology · 2020Review
- Recent advances into the role of pattern recognition receptors in transplantation.Cellular immunology · 2020Review
- Article
- Progenitor-derived human endothelial cells evade alloimmunity by CRISPR/Cas9-mediated complete ablation of MHC expression.JCI insight · 2019Article
- Complement Membrane Attack Complexes Assemble NLRP3 Inflammasomes Triggering IL-1 Activation of IFN-γ-Primed Human Endothelium.Circulation research · 2019Article
- ZFYVE21 is a complement-induced Rab5 effector that activates non-canonical NF-κB via phosphoinosotide remodeling of endosomes.Nature communications · 2019Article
- Complement-mediated Damage to the Glycocalyx Plays a Role in Renal Ischemia-reperfusion Injury in Mice.Transplantation direct · 2019Article
- Inhibition of the alternative complement pathway accelerates repair processes in the murine model of choroidal neovascularization.Molecular immunology · 2019Article
- NFκB and Kidney Injury.Frontiers in immunology · 2019Review
- Recent advances in allograft vasculopathy.Current opinion in organ transplantation · 2017Review
- Antibody Subclass Repertoire and Graft Outcome Following Solid Organ Transplantation.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Allograft vasculopathy (AV) is characterized by diffuse stenoses in the vasculature of solid organ transplants. Previously, we developed two humanized models showing that alloantibody and ischemia reperfusion injury (IRI) exacerbated T cell-mediated AV in human arterial xenografts in vivo. Herein we examined a causal role for terminal complement activation in both settings. IRI, in contrast to alloantibody, elicited widespread membrane attack complex (MAC) assembly throughout the vessel wall. Both alloantibody and IRI caused early (24 h) and robust endothelial cell (EC) activation localized to regions of intimal MAC deposition, indicated by increases in nuclear factor kappa B (NF-κB)-inducing kinase, an MAC-dependent activator of noncanonical NF-kB, VCAM-1 expression and Gr-1+ neutrophil infiltration. Endothelial cell activation by alloantibody was inhibited by antimouse C5 mAb, but not by anti-C5a mAb or by control mAb, implicating MAC as the primary target of anti-C5 mAb. Antimouse C5 mAb significantly reduced alloantibody- and IRI-enhanced T cell infiltration and AV-like changes, including neointimal hyperplasia as well as intraluminal thrombosis in a subset of IRI-treated arterial grafts. These results indicate that increased AV lesion formation in response to either alloantibody or IRI is dependent on complement C5 activation and, accordingly, inhibition of this pathway may attenuate AV.
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Registered trials
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