ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2014
Graft-derived CCL2 increases graft injury during antibody-mediated rejection of cardiac allografts.
Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Combination Automated Microfluidics Measurement of Urine C-C Motif Ligand 2, CXC-Motif Chemokine 9, CXC-Motif Chemokine 10, and Vascular Endothelial Growth Factor A for Monitoring Patients with a Kidney Transplant.Clinical journal of the American Society of Nephrology : CJASN · 2025Article
- Hypoxia inducible factor 2α promotes tolerogenic macrophage development during cardiac transplantation through transcriptional regulation of colony stimulating factor 1 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Human leukocyte antigen class I antibody-activated endothelium promotes CD206+ M2 macrophage polarization and MMP9 secretion through TLR4 signaling and P-selectin in a model of antibody-mediated rejection and allograft vasculopathy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- Review
- Heat shock protein 90 is a new potential target of anti-rejection therapy in allotransplantation.Cell stress & chaperones · 2022Article
- Bringing Clarity to the Murky Problem of Cardiac Allograft Vasculopathy.The American journal of pathology · 2022Article
- Molecular Signature of Antibody-Mediated Chronic Vasculopathy in Heart Allografts in a Novel Mouse Model.The American journal of pathology · 2022Article
- In the absence of natural killer cell activation donor-specific antibody mediates chronic, but not acute, kidney allograft rejection.Kidney international · 2019Article
- The Evolving Roles of Macrophages in Organ Transplantation.Journal of immunology research · 2019Review
- Integrated Proteome and Cytokine Profiles Reveal Ceruloplasmin Eliciting Liver Allograft Tolerance via Antioxidant Cascades.Frontiers in immunology · 2018Article
- Alcohol-Mediated Organ Damages: Heart and Brain.Frontiers in pharmacology · 2018Review
- MCP1 triggers monocyte dysfunctions during abnormal osteogenic differentiation of mesenchymal stem cells in ankylosing spondylitis.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Macrophages as Effectors of Acute and Chronic Allograft Injury.Current transplantation reports · 2016Article
- IL-1 Receptor Signaling on Graft Parenchymal Cells Regulates Memory and De Novo Donor-Reactive CD8 T Cell Responses to Cardiac Allografts.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Direct and indirect allograft recognition: pathways dictating graft rejection mechanisms.Current opinion in organ transplantation · 2016Review
- Heat Shock Protein 90α Is a Potential Serological Biomarker of Acute Rejection after Renal Transplantation.PloS one · 2016Article
- Antibodies to HLA Molecules Mimic Agonistic Stimulation to Trigger Vascular Cell Changes and Induce Allograft Injury.Current transplantation reports · 2015Article
- The divergent roles of macrophages in solid organ transplantation.Current opinion in organ transplantation · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The pathogenic role of macrophages in antibody-mediated rejection (AMR) remains unclear. Monocyte chemoattractant protein-1 (MCP-1/CCL2) is a potent chemotactic factor for monocytes and macrophages. The current studies used a murine model of AMR to investigate the role of graft-derived CCL2 in AMR and how macrophages may participate in antibody-mediated allograft injury. B6.CCR5−/−/CD8−/− recipients rejected MHC-mismatched WT A/J allografts with high donor-reactive antibody titers and diffuse C4d deposition in the large vessels and myocardial capillaries, features consistent with AMR. In contrast, A/J.CCL2−/− allografts induced low donor-reactive antibody titers and C4d deposition at Day 7 posttransplant. Decreased donor-reactive CD4 T cells producing interferon gamma were induced in response to A/J.CCL2−/− versus WT allografts. Consequently, A/J.CCL2−/− allograft survival was modestly but significantly longer than A/J allografts. Macrophages purified from WT allografts expressed high levels of IL-1β and IL-12p40 and this expression and the numbers of classically activated macrophages were markedly reduced in CCL2-deficient allografts on Day 7. The results indicate that allograft-derived CCL2 plays an important role in directing classically activated macrophages into allografts during AMR and that macrophages are important contributors to the inflammatory environment mediating graft tissue injury in this pathology, suggesting CCL2 as a therapeutic target for AMR.
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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.