Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (666 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Graft Rejections; Rejection, Graft; Rejections, Graft; Rejection, Transplant; Rejections, Transplant; Transplant Rejections; Transplant Rejection; Transplantation Rejection.
Where it fits in the MeSH classification
- Broader topics
- Host vs Graft Reaction
- See also
- Delayed Graft Function
Research landscape
PubMed indexes 68,521 records tagged with the MeSH heading “Graft Rejection” (counts retrieved 2026-10-29). 8,455 of them (12.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 27,348 records.
Reviews account for 10,437 records (15.2%) and meta-analyses for 464. Randomized controlled trials number 1,981 (2.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 27,348 |
| 2000-2009 | 15,868 |
| 2010-2019 | 16,850 |
| 2020 onward | 8,455 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 10,437 | 15.2% |
| Meta-analyses | 464 | 0.7% |
| Randomized controlled trials | 1,981 | 2.9% |
Method: PubMed query "Graft Rejection"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Injured epithelial cell states impact kidney allograft survival after T-cell-mediated rejection | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41605921 · DOI · PMC12852170 |
| Development and validation of a bronchoalveolar lavage genomic classifier for acute cellular rejection | 2025 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41337937 · DOI · PMC12719680 |
| Non-HLA antibody trajectories may predict kidney transplant outcomes | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41816322 · DOI · PMC12971436 |
Injured epithelial cell states impact kidney allograft survival after T-cell-mediated rejection [1]
Abstract reading summary — source excerpts
- Opening excerpt
- T-cell-mediated rejection (TCMR) remains a major cause of kidney transplant failure, despite being considered treatable.
- Closing excerpt
- Collectively, our results identify epithelial injury cell states as a determinant of outcome after TCMR.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (156 words)
T-cell-mediated rejection (TCMR) remains a major cause of kidney transplant failure, despite being considered treatable. Its impact reflects a limited understanding of the underlying molecular mechanisms and their clinical consequences. To address this, we induced acute TCMR in mouse kidney transplants and profiled molecular changes using single-nucleus RNA sequencing (snRNA-seq), spatial transcriptomics and immunofluorescence. Results were compared with human snRNA-seq data from TCMR and stable allografts, as well as single-cell deconvolution analysis of bulk transcriptomic data from kidney transplant biopsies. Here we show that TCMR induces injured epithelial cell states in mouse kidney allografts, particularly in proximal tubules and thick ascending limbs. Spatial transcriptomics of these injured epithelial states demonstrated heterogeneous localization, interactions with immune cells and cellular microenvironments. Cross-species analysis confirmed similar severely injured epithelial states in human samples, whose abundances correlated with transplant survival and persisted despite TCMR resolution. Collectively, our results identify epithelial injury cell states as a determinant of outcome after TCMR.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41605921 · DOI · PMC12852170
Development and validation of a bronchoalveolar lavage genomic classifier for acute cellular rejection [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundAcute cellular rejection (ACR) is the main risk factor for chronic lung allograft dysfunction (CLAD), but diagnosis requires invasive transbronchial biopsy (TBB).
- Closing excerpt
- FundingThis study was supported by the National Institute of Allergy and Infectious Diseases awards U01AI113315 and U01AI0635594, the Cystic Fibrosis Foundation award PALMER19AB0, and the Saul and Joyce Brandman Foundation Center for Lung Health at UCLA.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (252 words)
BackgroundAcute cellular rejection (ACR) is the main risk factor for chronic lung allograft dysfunction (CLAD), but diagnosis requires invasive transbronchial biopsy (TBB). We previously demonstrated the feasibility of bronchoalveolar lavage cell pellet (BAL-cp) gene expression for ACR diagnosis. We sought to develop and validate a genomic classifier for ACR in a multicenter cohort.MethodsWe performed RNA-seq on 806 BAL-cp from 181 lung transplant recipients enrolled in CTOT-20. Differential expression was based on fold difference >2.0 and False Discovery adjusted p-value FindingsFrom 37 clinically significant ACR and 151 stable control samples, we identified 62 ACR genes, indicating upregulation of T-cell receptor signalling, and downregulation of CTLA4 signalling in cytotoxic lymphocytes, among other enriched pathways. A 31-gene Random Forest model's AUC was 0.99 (SE 0.0053) in the training set, and 0.72 (SE 0.0874) in the test set. At a probability threshold of 0.396, accuracy for distinguishing clinically significant ACR cases from stable controls was 93.1% (specificity 95.4%, sensitivity 83.8%). In the independent validation cohort, accuracy was 82.1% (specificity 87.5%, sensitivity 73.3%). The model classified 138 (17.1%) CTOT-20 samples as genomic ACR. Late genomic ACR (≥90 days posttransplant) associated with increased CLAD risk (HR 2.52, 95% CI 1.47-4.34, p InterpretationA BAL-cp genomic classifier can identify ACR, predict CLAD risk, and may be a less invasive alternative to TBB after lung transplant.FundingThis study was supported by the National Institute of Allergy and Infectious Diseases awards U01AI113315 and U01AI0635594, the Cystic Fibrosis Foundation award PALMER19AB0, and the Saul and Joyce Brandman Foundation Center for Lung Health at UCLA.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41337937 · DOI · PMC12719680
Non-HLA antibody trajectories may predict kidney transplant outcomes [3]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionDonor-specific HLA antibodies (DSAs) are well-established mediators of antibody-mediated rejection (AMR), but growing evidence suggests that non-HLA antibodies may also contribute to kidney allograft dysfunction.
- Closing excerpt
- Larger multicenter studies are needed to define clinically meaningful threshold and estabilish the utility of non-HLA PRA testing across diverse transplant populations.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (258 words)
IntroductionDonor-specific HLA antibodies (DSAs) are well-established mediators of antibody-mediated rejection (AMR), but growing evidence suggests that non-HLA antibodies may also contribute to kidney allograft dysfunction. However, the clinical utility of non-HLA antibody testing remains limited due to assay variability and undefined pathogenic thresholds.MethodsIn this longitudinal study, we evaluated 167 deceased-donor kidney transplant recipients at UCSF using a multiplex Luminex assay to quantify IgG reactivity against 88 non-HLA antigens in paired pre- and post-transplant serum samples (n = 334). Patients were stratified by HLA-DSA status and graft outcome. The non-HLA panel reactive antibody (PRA) percentage was defined as the proportion of positive beads among the 88 tested antigens.ResultsGlobal non-HLA PRA declined significantly from pre- to post-transplant (9% to 6%; P = 0.0010) only among recipients with functioning grafts, driven by reduced reactivity to signaling, cytoskeletal, and immune-related antigens. Elevated pre-transplant non-HLA PRA was associated with prior sensitization, IgA nephropathy, and African American ancestry, but was independent of age, ABO type, and HLA cPRA. AMR occurred primarily in recipients with both preformed and de novo DSA, while no rejection was observed in DSA-negative recipients. Death-censored graft survival varied across groups, and neither preformed nor de novo DSA consistently predicted outcomes.DiscussionThese findings suggest that longitudinal trajectories of non-HLA PRA, rather than staticmeasurements or DSA status alone, may influence graft loss. The dynamic nature of non-HLA antibody responses and supports integration of non-HLA antibody profiling into longitudinal immune monitoring frameworks. Larger multicenter studies are needed to define clinically meaningful threshold and estabilish the utility of non-HLA PRA testing across diverse transplant populations.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41816322 · DOI · PMC12971436
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Regulatory cell therapy in kidney transplantation (The ONE Study): a harmonised design and analysis of seven non-randomised, single-arm, phase 1/2A trials [4]
- Research article Assessing relative risks of infection and rejection: a meta-analysis using an immune function assay [5]
- Research article Corneal neovascularization as a risk factor for graft failure and rejection after keratoplasty: an evidence-based meta-analysis [6]
- Research article Azathioprine and Risk of Skin Cancer in Organ Transplant Recipients: Systematic Review and Meta-Analysis [7]
- Research article What is the impact of hypogammaglobulinemia on the rate of infections and survival in solid organ transplantation? A meta-analysis [8]
- Research article The Treatment of Antibody-Mediated Rejection in Kidney Transplantation: An Updated Systematic Review and Meta-Analysis [9]
References
- Pfefferkorn AM, Jahn L, Gauthier PT, Kulow VA, Roeles J, Müller-Bötticher N, et al.. Injured epithelial cell states impact kidney allograft survival after T-cell-mediated rejection. . 2026. PMID 41605921 · DOI · PMC12852170
- Weigt SS, Zhou J, Okuno T, Neely ML, Lari S, Palchevskiy V, et al.. Development and validation of a bronchoalveolar lavage genomic classifier for acute cellular rejection. . 2025. PMID 41337937 · DOI · PMC12719680
- Rajalingam R, Sigdel TK, Maruthamuthu S, Raghav PK, Laszik ZG, Da Gente G, et al.. Non-HLA antibody trajectories may predict kidney transplant outcomes. . 2026. PMID 41816322 · DOI · PMC12971436
- Sawitzki B, Harden PN, Reinke P, Moreau A, Hutchinson JA, Game DS, et al.. Regulatory cell therapy in kidney transplantation (The ONE Study): a harmonised design and analysis of seven non-randomised, single-arm, phase 1/2A trials. Lancet. 2020. PMID 32446407 · DOI · PMC7613154
- Kowalski RJ, Post DR, Mannon RB, Sebastian A, Wright HI, Sigle G, et al.. Assessing relative risks of infection and rejection: a meta-analysis using an immune function assay. Transplantation. 2006. PMID 16969290 · DOI
- Bachmann B, Taylor RS, Cursiefen C. Corneal neovascularization as a risk factor for graft failure and rejection after keratoplasty: an evidence-based meta-analysis. Ophthalmology. 2010. PMID 20605214 · DOI
- Jiyad Z, Olsen CM, Burke MT, Isbel NM, Green AC. Azathioprine and Risk of Skin Cancer in Organ Transplant Recipients: Systematic Review and Meta-Analysis. Am J Transplant. 2016. PMID 27163483 · DOI
- Florescu DF, Kalil AC, Qiu F, Schmidt CM, Sandkovsky U. What is the impact of hypogammaglobulinemia on the rate of infections and survival in solid organ transplantation? A meta-analysis. Am J Transplant. 2013. PMID 23919557 · DOI
- Wan SS, Ying TD, Wyburn K, Roberts DM, Wyld M, Chadban SJ. The Treatment of Antibody-Mediated Rejection in Kidney Transplantation: An Updated Systematic Review and Meta-Analysis. Transplantation. 2018. PMID 29315141 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.