ArticleBiomedicines2022
The Proteome of Antibody-Mediated Rejection: From Glomerulitis to Transplant Glomerulopathy.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- A Subset of Pro-inflammatory CXCL10+ LILRB2+ Macrophages Derives From Recipient Monocytes and Drives Renal Allograft Rejection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Advances in antibody-mediated rejection of renal allografts.Frontiers in immunology · 2026Review
- Identification of RNA-binding protein genes associated with renal rejection and graft survival.Renal failure · 2024Article
- Article
- Molecular landscape of kidney allograft tissues data integration portal (NephroDIP): a curated database to improve integration of high-throughput kidney transplant datasets.Frontiers in immunology · 2024Article
- Transcriptional and spatial profiling of the kidney allograft unravels a central role for FcyRIII+ innate immune cells in rejection.Nature communications · 2023Article
- Biomarker-Development Proteomics in Kidney Transplantation: An Updated Review.International journal of molecular sciences · 2023Review
- Mass spectrometry-based proteomics for advancing solid organ transplantation research.Frontiers in transplantation · 2023Review
- Periostin as a Biomarker in the Setting of Glomerular Diseases-A Review of the Current Literature.Biomedicines · 2022Review
- WARS1, TYMP and GBP1 display a distinctive microcirculation pattern by immunohistochemistry during antibody-mediated rejection in kidney transplantation.Scientific reports · 2022Article
- Glomerulitis in T cell-mediated renal allograft rejection and antibody-mediated rejection histology in the absence of donor-specific antibodies heralds a similar clinico-morphologic pattern of injury to an antibody-mediated rejection: A systematic review.Medical journal, Armed Forces IndiaReview
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Antibody-mediated rejection (ABMR) is the leading cause of allograft failure in kidney transplantation. Its histological hallmark is represented by lesions of glomerulitis i.e., inflammatory cells within glomeruli. Current therapies for ABMR fail to prevent chronic allograft damage i.e., transplant glomerulopathy, leading to allograft loss. We used laser microdissection of glomeruli from formalin-fixed allograft biopsies combined with mass spectrometry-based proteomics to describe the proteome modification of 11 active and 10 chronic active ABMR cases compared to 8 stable graft controls. Of 1335 detected proteins, 77 were deregulated in glomerulitis compared to stable grafts, particularly involved in cellular stress mediated by interferons type I and II, leukocyte activation and microcirculation remodeling. Three proteins extracted from this protein profile, TYMP, WARS1 and GBP1, showed a consistent overexpression by immunohistochemistry in glomerular endothelial cells that may represent relevant markers of endothelial stress during active ABMR. In transplant glomerulopathy, 137 proteins were deregulated, which favor a complement-mediated mechanism, wound healing processes through coagulation activation and ultimately a remodeling of the glomerular extracellular matrix, as observed by light microscopy. This study brings novel information on glomerular proteomics of ABMR in kidney transplantation, and highlights potential targets of diagnostic and therapeutic interest.
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