ArticleThe American journal of pathology2011
Complement regulates CD4 T-cell help to CD8 T cells required for murine allograft rejection.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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
38 citing papers in PubMed, 59 citations in OpenAlex.
- Article
- Emerging roles for complement in lung transplantation.The Journal of clinical investigation · 2025Review
- Role of intrarenal complement production in kidney transplantation.Clinical kidney journal · 2025Review
- Critical Role of CD55 in Controlling Wound Healing.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Complementing Testicular Immune Regulation: The Relationship between Sertoli Cells, Complement, and the Immune Response.International journal of molecular sciences · 2023Review
- Mannan-Binding Lectin Promotes Murine Graft-versus-Host Disease by Amplifying Lipopolysaccharide-Initiated Inflammation.Transplantation and cellular therapy · 2022Article
- Graft rejection markers in children undergoing hematopoietic cell transplant for bone marrow failure.Blood advances · 2021Article
- A novel injury site-natural antibody targeted complement inhibitor protects against lung transplant injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Article
- Sterile inflammation in thoracic transplantation.Cellular and molecular life sciences : CMLS · 2021Review
- Recent advances into the role of pattern recognition receptors in transplantation.Cellular immunology · 2020Review
- The Immunological Basis of Liver Allograft Rejection.Frontiers in immunology · 2020Review
- Linking innate immunity and chronic antibody-mediated allograft rejection.Current opinion in organ transplantation · 2019Review
- Absence of recipient C3aR1 signaling limits expansion and differentiation of alloreactive CD8American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019Article
- 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
- Inhibition of Autophagy Prolongs Recipient Survival Through Promoting CD8Frontiers in immunology · 2019Article
- C5aR1 regulates T follicular helper differentiation and chronic graft-versus-host disease bronchiolitis obliterans.JCI insight · 2018Article
- Donor pretreatment with nebulized complement C3a receptor antagonist mitigates brain-death induced immunological injury post-lung transplant.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018Article
- Understanding the Correlation Between DSA, Complement Activation, and Antibody-Mediated Rejection in Heart Transplant Recipients.Transplantation · 2018Article
- Polymyositis as a manifestation of chronic graft-versus-host disease after allo-HSCT.Clinical case reports · 2018Article
- T Cell Expression of C5a Receptor 2 Augments Murine Regulatory T Cell (TJournal of immunology (Baltimore, Md. : 1950) · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Although induction of CD8 T-cell responses to transplants requires CD4-cell help, how this help is transmitted remains incompletely characterized. In vitro, cognate interactions between CD4 T cells and dendritic cells (DCs) induce C3a and C5a production. CD8(+) T cells lacking C3a receptor (C3aR) and C5a receptor (C5aR) proliferate weakly to allogeneic DCs despite CD4 help, indicating that CD4-cell help is mediated, in part, through DC-derived C3a/C5a acting on CD8(+) T cell-expressed C3aR/C5aR. In support of this concept, augmenting DC C5a/C3a production bypasses the requirement for CD4- and CD40-dependent help to wild-type CD8(+) T cells. CD4-deficient recipients of allogeneic heart transplants prime weak CD8 responses and do not acutely reject their grafts. In contrast, CD4-deficient chimeric mice possessing decay accelerating factor deficient (Daf1(-/-)) bone marrow, in which DC C3a/C5a production is potentiated, acutely reject transplants through a CD8 cell-dependent mechanism. Furthermore, hearts transplanted into CD40(-/-) mice prime weak CD8-cell responses and survive indefinitely, but hearts transplanted into Daf1(-/-)CD40(-/-) recipients undergo CD8 cell-dependent rejection. Together, the data indicate that heightened production and activation of immune cell-derived complement bypasses the need for CD40/CD154 interactions and implicate antigen-presenting cell-produced C5a and C3a as molecular bridges linking CD4 help to CD8(+) T cells.
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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.