ArticleJCI insight2020
Single cell transcriptomics of mouse kidney transplants reveals a myeloid cell pathway for transplant rejection.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Donor macrophage depletion permits posttransplant tolerance induction in a murine islet transplant model.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Application of machine learning in the research progress of post-kidney transplant rejection.World journal of transplantation · 2026Review
- Nicheformer: a foundation model for single-cell and spatial omics.Nature methods · 2025Article
- Article
- Defensive tolerance drives the reprogramming and dysfunction of infiltrating pathogenic B cells assuring the maintenance of tolerance.Research square · 2025Article
- Discovering molecular signatures in kidney transplant biopsies with borderline changes and isolated V-lesions: single-cell RNA-sequencing analysis of human blood and tissue Spatial transcriptomics.Scientific reports · 2025Article
- The crucial role of metabolic reprogramming in driving macrophage conversion in kidney disease.Cellular & molecular biology letters · 2025Review
- Unraveling the Roles of Macrophages in Vascularized Composite Allotransplantation.Biomedicines · 2025Review
- Senescence-induced p21Cell discovery · 2025Article
- Graft-derived extracellular vesicles transport miRNAs to modulate macrophage polarization after heart transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025Article
- Identification and characterization of senescent macrophages in renal allograft rejection: a cross-species MultiOmics study.Frontiers in immunology · 2025Article
- Single-cell transcriptomics unravels the early immune landscape of renal allograft rejection and nominates Ccl3-Ccr5 as a therapeutic target.Frontiers in immunology · 2025Article
- Optimization of mouse kidney digestion protocols for single-cell applications.Physiological genomics · 2024Article
- Single-Cell RNA Sequencing in Organ and Cell Transplantation.Biosensors · 2024Review
- AXL inhibition suppresses early allograft monocyte-to-macrophage differentiation and prolongs allograft survival.JCI insight · 2024Article
- Dissecting the immune discrepancies in mouse liver allograft tolerance and heart/kidney allograft rejection.Cell proliferation · 2024Article
- Deciphering the Complexity of the Immune Cell Landscape in Kidney Allograft Rejection.Transplant international : official journal of the European Society for Organ Transplantation · 2024Review
- Assessing GPT-4 for cell type annotation in single-cell RNA-seq analysis.bioRxiv : the preprint server for biology · 2023Article
- Multi-omics Approach in Kidney Transplant: Lessons Learned from COVID-19 Pandemic.Current transplantation reports · 2023Article
- Reference-free and cost-effective automated cell type annotation with GPT-4 in single-cell RNA-seq analysis.Research square · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Myeloid cells are increasingly recognized as major players in transplant rejection. Here, we used a murine kidney transplantation model and single cell transcriptomics to dissect the contribution of myeloid cell subsets and their potential signaling pathways to kidney transplant rejection. Using a variety of bioinformatic techniques, including machine learning, we demonstrate that kidney allograft-infiltrating myeloid cells followed a trajectory of differentiation from monocytes to proinflammatory macrophages, and they exhibited distinct interactions with kidney allograft parenchymal cells. While this process correlated with a unique pattern of myeloid cell transcripts, a top gene identified was Axl, a member of the receptor tyrosine kinase family Tyro3/Axl/Mertk (TAM). Using kidney transplant recipients with Axl gene deficiency, we further demonstrate that Axl augmented intragraft differentiation of proinflammatory macrophages, likely via its effect on the transcription factor Cebpb. This, in turn, promoted intragraft recruitment, differentiation, and proliferation of donor-specific T cells, and it enhanced early allograft inflammation evidenced by histology. We conclude that myeloid cell Axl expression identified by single cell transcriptomics of kidney allografts in our study plays a major role in promoting intragraft myeloid cell and T cell differentiation, and it presents a potentially novel therapeutic target for controlling kidney allograft rejection and improving kidney allograft survival.
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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.