ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Tolerogenic Donor-Derived Dendritic Cells Risk Sensitization In Vivo owing to Processing and Presentation by Recipient APCs.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
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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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Effects of Adoptive Transfer of Tolerogenic Dendritic Cells on Allograft Survival in Organ Transplantation Models: An Overview of Systematic Reviews.Journal of immunology research · 2016Pooled it
- Restoring Immunological Tolerance via Dendritic Cells in Rheumatoid Arthritis.European journal of immunology · 2026Review
- Targeting Recipient Dendritic Cells with Sialic Acid-Modified Donor Alloantigen Prolongs Skin Transplant Survival.International journal of molecular sciences · 2025Article
- The inhibitory receptor Siglec-E controls antigen-presenting cell activation and T cell-mediated transplant rejection.Science translational medicine · 2025Article
- Detection and Monitoring of Regulatory Immune Cells Following Their Adoptive Transfer in Organ Transplantation.Frontiers in immunology · 2020Review
- Localized delivery of immunosuppressive regulatory T cells to peripheral nerve allografts promotes regeneration of branched segmental defects.Biomaterials · 2019Article
- Optimal Tolerogenic Dendritic Cells in Type 1 Diabetes (T1D) Therapy: What Can We Learn From Non-obese Diabetic (NOD) Mouse Models?Frontiers in immunology · 2019Review
- March1-dependent modulation of donor MHC II on CD103Nature communications · 2018Article
- Regulatory T cell-derived extracellular vesicles modify dendritic cell function.Scientific reports · 2018Article
- Effect of immune tolerance induced by immature dendritic cells and CTLA4-Ig on systemic lupus erythematosus: AnExperimental and therapeutic medicine · 2018Article
- Galectin-1 is required for the regulatory function of B cells.Scientific reports · 2018Article
- Antigen Loading (e.g., Glutamic Acid Decarboxylase 65) of Tolerogenic DCs (tolDCs) Reduces Their Capacity to Prevent Diabetes in the Non-Obese Diabetes (NOD)-Severe Combined Immunodeficiency Model of Adoptive Cotransfer of Diabetes As Well As in NOD Mice.Frontiers in immunology · 2018Article
- Harnessing Apoptotic Cells for Transplantation Tolerance: Current Status and Future Perspectives.Current transplantation reports · 2017Article
- Constitutive expression of the anti-apoptotic Bcl-2 family member A1 in murine endothelial cells leads to transplant tolerance.Clinical and experimental immunology · 2017Article
- Update on Dendritic Cell-Induced Immunological and Clinical Tolerance.Frontiers in immunology · 2017Review
- Immunosuppressive human anti-CD83 monoclonal antibody depletion of activated dendritic cells in transplantation.Leukemia · 2016Article
- Diversity of gut microflora is required for the generation of B cell with regulatory properties in a skin graft model.Scientific reports · 2015Article
- Tempering allorecognition to induce transplant tolerance with chemically modified apoptotic donor cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015Review
- Orchestration of transplantation tolerance by regulatory dendritic cell therapy or in-situ targeting of dendritic cells.Current opinion in organ transplantation · 2014Review
- Transplantation tolerance and its outcome during infections and inflammation.Immunological reviews · 2014Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Modification of allogeneic dendritic cells (DCs) through drug treatment results in DCs with in vitro hallmarks of tolerogenicity. Despite these observations, using murine MHC-mismatched skin and heart transplant models, donor-derived drug-modified DCs not only failed to induce tolerance but also accelerated graft rejection. The latter was inhibited by injecting the recipient with anti-CD8 Ab, which removed both CD8(+) T cells and CD8(+) DCs. The discrepancy between in vitro and in vivo data could be explained, partly, by the presentation of drug-modified donor DC MHC alloantigens by recipient APCs and activation of recipient T cells with indirect allospecificity, leading to the induction of alloantibodies. Furthermore, allogeneic MHC molecules expressed by drug-treated DCs were rapidly processed and presented in peptide form by recipient APCs in vivo within hours of DC injection. Using TCR-transgenic T cells, Ag presentation of injected OVA-pulsed DCs was detectable for ≤ 3 d, whereas indirect presentation of MHC alloantigen by recipient APCs led to activation of T cells within 14 h and was partially inhibited by reducing the numbers of CD8(+) DCs in vivo. In support of this observation when mice lacking CD8(+) DCs were pretreated with drug-modified DCs prior to transplantation, skin graft rejection kinetics were similar to those in non-DC-treated controls. Of interest, when the same mice were treated with anti-CD40L blockade plus drug-modified DCs, skin graft survival was prolonged, suggesting endogenous DCs were responsible for T cell priming. Altogether, these findings highlight the risks and limitations of negative vaccination using alloantigen-bearing "tolerogenic" DCs.
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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.