ArticleThe Journal of clinical investigation2023
Multiscale genetic architecture of donor-recipient differences reveals intronic LIMS1 mismatches associated with kidney transplant survival.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Genome-wide donor-recipient non-HLA mismatch and graft loss.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Pooled it
- APOL1 risk alleles modulate T cell receptor signaling to promote allograft rejection.The Journal of clinical investigation · 2026Article
- The Impact of Complement Factor H-Related Protein Gene Deletions on Kidney Transplantation.Scandinavian journal of immunology · 2025Article
- Non-HLA Genetics and Application to Living Donor Candidates.Current transplantation reports · 2025Article
- Genomics in Pancreas-Kidney Transplantation: From Risk Stratification to Personalized Medicine.Genes · 2025Review
- Regulatory T cells in kidney transplant recipients with LIMS1 rs893403 risk genotype.Clinical transplantation · 2024Article
- Polygenic risk score for acute rejection based on donor-recipient non-HLA genotype mismatch.PloS one · 2024Article
- Novel Aspects of Immunogenetics and Post-Transplant Events in Kidney Transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2024Review
Corrections and comments
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Authors and funding
18 authors at 9 institutions in 5 countries.
Funding
Abstract
Donor-recipient (D-R) mismatches outside of human leukocyte antigens (HLAs) contribute to kidney allograft loss, but the mechanisms remain unclear, specifically for intronic mismatches. We quantified non-HLA mismatches at variant-, gene-, and genome-wide scales from single nucleotide polymorphism (SNP) data of D-Rs from 2 well-phenotyped transplant cohorts: Genomics of Chronic Allograft Rejection (GoCAR; n = 385) and Clinical Trials in Organ Transplantation-01/17 (CTOT-01/17; n = 146). Unbiased gene-level screening in GoCAR uncovered the LIMS1 locus as the top-ranked gene where D-R mismatches associated with death-censored graft loss (DCGL). A previously unreported, intronic, LIMS1 haplotype of 30 SNPs independently associated with DCGL in both cohorts. Haplotype mismatches showed a dosage effect, and minor-allele introduction to major-allele-carrying recipients showed greater hazard of DCGL. The LIMS1 haplotype and the previously reported LIMS1 SNP rs893403 are expression quantitative trait loci (eQTL) in immune cells for GCC2 (not LIMS1), which encodes a protein involved in mannose-6-phosphase receptor (M6PR) recycling. Peripheral blood and T cell transcriptome analyses associated the GCC2 gene and LIMS1 SNPs with the TGF-β1/SMAD pathway, suggesting a regulatory effect. In vitro GCC2 modulation impacted M6PR-dependent regulation of active TGF-β1 and downstream signaling in T cells. Together, our data link LIMS1 locus D-R mismatches to DCGL via GCC2 eQTLs that modulate TGF-β1-dependent effects on T cells.
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Registered trials
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