ArticleNature communications2023
Transcriptional and spatial profiling of the kidney allograft unravels a central role for FcyRIII+ innate immune cells in rejection.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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.
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Who cites it
65 citing papers in PubMed, 112 citations in OpenAlex.
- Artificial Intelligence in Kidney Transplant Pathology: Current Evidence, Limitations, and Relevance to the Banff Framework.Kidney international reports · 2026Review
- Article
- Integration of Bulk and Single-Cell RNA Sequencing Analyses in Biomedicine.International journal of molecular sciences · 2026Review
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Natural killer cells in kidney immune surveillance, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- Dual inhibition of mTOR and calcineurin pathways mitigates missing self-induced NK cell-mediated microvascular rejection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- A Subset of Pro-inflammatory CXCL10+ LILRB2+ Macrophages Derives From Recipient Monocytes and Drives Renal Allograft Rejection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- BHLHE40 Orchestrates Effector Tissue-Resident Memory CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondria in Renal Ischemia-Reperfusion Injury: From Mechanisms to Therapeutics.Biomedicines · 2026Review
- The honeybee gut microbiome: a novel multidimensional model of antimicrobial resistance transmission and immune homeostasis from environmental interactions to health regulation.FEMS microbiology reviews · 2026Review
- Bone Marrow-Derived Macrophage NLRP3 Mediates Renal Fibrosis by triggering TGF-β/Smad3-mediated Macrophage-Myofibroblast Transition.International journal of biological sciences · 2026Article
- Innovative approaches targeting innate immune cells to promote organ transplant tolerance.Frontiers in transplantation · 2026Review
- Single-cell transcriptomic landscape of metabolic reprogramming in kidney allograft rejection.Frontiers in immunology · 2026Article
- Pathogenesis of Chronic Rejection: Graft Endothelial Cell Trans-presentation of IL-15 Connects Alloantibody- and Cell-Mediated Steps in Allograft Vasculopathy.Results and problems in cell differentiation · 2026Review
- Innate-immune crosstalk orchestrates T cell-mediated rejection in kidney transplants.Frontiers in immunology · 2026Article
- Evolving Therapeutic Approaches for Treatment of Antibody-Mediated Rejection in Renal Allograft Recipients.Results and problems in cell differentiation · 2026Review
- Molecular diagnostics in pancreas transplantation: past, present, and future.Frontiers in molecular biosciences · 2026Review
- One tool, multiple gains: anti-CD38 therapy in antibody-mediated rejection.Clinical kidney journal · 2025Article
- Multiplex Immunofluorescence Assay with Opal Reagents for Identifying Mononuclear Cell Subsets in Kidney Allograft Rejection Types.International journal of molecular sciences · 2025Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
31 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rejection remains the main cause of premature graft loss after kidney transplantation, despite the use of potent immunosuppression. This highlights the need to better understand the composition and the cell-to-cell interactions of the alloreactive inflammatory infiltrate. Here, we performed droplet-based single-cell RNA sequencing of 35,152 transcriptomes from 16 kidney transplant biopsies with varying phenotypes and severities of rejection and without rejection, and identified cell-type specific gene expression signatures for deconvolution of bulk tissue. A specific association was identified between recipient-derived FCGR3A+ monocytes, FCGR3A+ NK cells and the severity of intragraft inflammation. Activated FCGR3A+ monocytes overexpressed CD47 and LILR genes and increased paracrine signaling pathways promoting T cell infiltration. FCGR3A+ NK cells overexpressed FCRL3, suggesting that antibody-dependent cytotoxicity is a central mechanism of NK-cell mediated graft injury. Multiplexed immunofluorescence using 38 markers on 18 independent biopsy slides confirmed this role of FcγRIII+ NK and FcγRIII+ nonclassical monocytes in antibody-mediated rejection, with specificity to the glomerular area. These results highlight the central involvement of innate immune cells in the pathogenesis of allograft rejection and identify several potential therapeutic targets that might improve allograft longevity.
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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.