ArticleJournal of the American Society of Nephrology : JASN2012
Absence of MyD88 signaling induces donor-specific kidney allograft tolerance.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 57 citations in OpenAlex.
- Can mouse kidney transplant models inform mechanisms of injury and acceptance in clinical kidney transplantation?American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025Review
- Insight on immune cells in rejection and infection postlung transplant.Immunity, inflammation and disease · 2023Review
- The aging of the immune system and its implications for transplantation.GeroScience · 2023Review
- Review
- Methods to Study TLRs in Transplantation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Assessment of Physiological Rat Kidney Ageing-Implications for the Evaluation of Allograft Quality Prior to Renal Transplantation.Metabolites · 2022Article
- Donor-derived Cell-free DNA: Advancing a Novel Assay to New Heights in Renal Transplantation.Transplantation direct · 2021Article
- Untangling Local Pro-Inflammatory, Reparative, and Regulatory Damage-Associated Molecular-Patterns (DAMPs) Pathways to Improve Transplant Outcomes.Frontiers in immunology · 2021Review
- Renoprotective Effects of Maslinic Acid on Experimental Renal Fibrosis in Unilateral Ureteral Obstruction Model via Targeting MyD88.Frontiers in pharmacology · 2021Article
- Gut Microbial Metabolites Induce Donor-Specific Tolerance of Kidney Allografts through Induction of T Regulatory Cells by Short-Chain Fatty Acids.Journal of the American Society of Nephrology : JASN · 2020Article
- Article
- Is There a Role for Natural Antibodies in Rejection Following Transplantation?Transplantation · 2019Review
- Inhibition of intimal hyperplasia in murine aortic allografts by administration of a small-molecule TLR4 inhibitor TAK-242.Scientific reports · 2017Article
- Danger signals in regulating the immune response to solid organ transplantation.The Journal of clinical investigation · 2017Review
- Aging and the immune response to organ transplantation.The Journal of clinical investigation · 2017Review
- Inhibition of Myeloid Differentiation Factor 88 Reduces Human and Mouse T-Cell Interleukin-17 and IFNγ Production and Ameliorates Experimental Autoimmune Encephalomyelitis Induced in Mice.Frontiers in immunology · 2017Article
- Innate immune mechanisms in transplant allograft vasculopathy.Current opinion in organ transplantation · 2016Review
- Role of TLRs and DAMPs in allograft inflammation and transplant outcomes.Nature reviews. Nephrology · 2016Review
- Recipient Myd88 Deficiency Promotes Spontaneous Resolution of Kidney Allograft Rejection.Journal of the American Society of Nephrology : JASN · 2015Article
- How the Innate Immune System Senses Trouble and Causes Trouble.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) play a fundamental role in innate immunity and provide a link between innate and adaptive responses to an allograft; however, whether the development of acute and chronic allograft rejection requires TLR signaling is unknown. Here, we studied TLR signaling in a fully MHC-mismatched, life-sustaining murine model of kidney allograft rejection. Mice deficient in the TLR adaptor protein MyD88 developed donor antigen-specific tolerance, which protected them from both acute and chronic allograft rejection and increased their survival after transplantation compared with wild-type controls. Administration of an anti-CD25 antibody to MyD88-deficient recipients depleted CD4(+)CD25(+)FoxP3(+) cells and broke tolerance. In addition, defective development of Th17 immune responses to alloantigen both in vitro and in vivo occurred, resulting in an increased ratio of Tregs to Th17 effectors. Thus, MyD88 deficiency was associated with an altered balance of Tregs over Th17 cells, promoting tolerance instead of rejection. This study provides evidence that targeting innate immunity may be a clinically relevant strategy to facilitate transplantation tolerance.
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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.