ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Donor deficiency of decay-accelerating factor accelerates murine T cell-mediated cardiac allograft rejection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 92 citations in OpenAlex.
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Role of intrarenal complement production in kidney transplantation.Clinical kidney journal · 2025Review
- Graft rejection in paediatric congenital heart disease.Translational pediatrics · 2023Review
- Review
- Complement-targeted therapies in kidney transplantation-insights from preclinical studies.Frontiers in immunology · 2022Review
- Sterile inflammation in thoracic transplantation.Cellular and molecular life sciences : CMLS · 2021Review
- Hypoxia-induced complement dysregulation is associated with microvascular impairments in mouse tracheal transplants.Journal of translational medicine · 2020Article
- C5aR1 regulates migration of suppressive myeloid cells required for costimulatory blockade-induced murine allograft survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019Article
- Role of Complement Activation in Allograft Inflammation.Current transplantation reports · 2019Article
- Complement and Transplantation: From New Mechanisms to Potential Biomarkers and Novel Treatment Strategies.Clinics in laboratory medicine · 2019Review
- C5aR1 regulates T follicular helper differentiation and chronic graft-versus-host disease bronchiolitis obliterans.JCI insight · 2018Article
- Targeting complement-mediated immunoregulation for cancer immunotherapy.Seminars in immunology · 2018Review
- Complement and the Regulation of T Cell Responses.Annual review of immunology · 2018Review
- TLR-Induced Murine Dendritic Cell (DC) Activation Requires DC-Intrinsic Complement.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Production of complement components by cells of the immune system.Clinical and experimental immunology · 2017Review
- Complement in Kidney Transplantation.Frontiers in medicine · 2017Review
- The "ins and outs" of complement-driven immune responses.Immunological reviews · 2016Review
- What Is Direct Allorecognition?Current transplantation reports · 2016Review
- Antibody Subclass Repertoire and Graft Outcome Following Solid Organ Transplantation.Frontiers in immunology · 2016Review
- Molecules Great and Small: The Complement System.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Decay-accelerating factor (DAF) is a cell surface regulator that accelerates the dissociation of C3/C5 convertases and thereby prevents the amplification of complement activation on self cells. In the context of transplantation, DAF has been thought to primarily regulate antibody-mediated allograft injury, which is in part serum complement-dependent. Based on our previously delineated link between DAF and CD4 T cell responses, we evaluated the effects of donor Daf1 (the murine homolog of human DAF) deficiency on CD8 T cell-mediated cardiac allograft rejection. MHC-disparate Daf1(-/-) allografts were rejected with accelerated kinetics compared with wild-type grafts. The accelerated rejection predominantly tracked with DAF's absence on bone marrow-derived cells in the graft and required allograft production of C3. Transplantation of Daf1(-/-) hearts into wild-type allogeneic hosts augmented the strength of the anti-donor (direct pathway) T cell response, in part through complement-dependent proliferative and pro-survival effects on alloreactive CD8 T cells. The accelerated allograft rejection of Daf1(-/-) hearts occurred in recipients lacking anti-donor Abs. The results reveal that donor DAF expression, by controlling local complement activation on interacting T cell APC partners, regulates the strength of the direct alloreactive CD8(+) T cell response. The findings provide new insights into links between innate and adaptive immunity that could be exploited to limit T cell-mediated injury to an allograft following transplantation.
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What OpenQuestion holds
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.