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: 4 complete abstracts (920 words), 10 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
The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the graft VS host reaction.
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: Runt Disease; Disease, Runt; Graft-Versus-Host Disease; Disease, Graft-Versus-Host; Diseases, Graft-Versus-Host; Graft Versus Host Disease; Graft-Versus-Host Diseases; Graft-vs-Host Disease.
Where it fits in the MeSH classification
- Broader topics
- Immune System Diseases
- Narrower topics
- Bronchiolitis Obliterans Syndrome
Related concepts
- Transplants
- Host Reaction
Research landscape
PubMed indexes 30,648 records tagged with the MeSH heading “Graft vs Host Disease” (counts retrieved 2026-10-29). 7,616 of them (24.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 9,115 records.
Reviews account for 5,223 records (17.0%) and meta-analyses for 206. Randomized controlled trials number 550 (1.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 6,745 |
| 2000-2009 | 7,172 |
| 2010-2019 | 9,115 |
| 2020 onward | 7,616 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,223 | 17.0% |
| Meta-analyses | 206 | 0.7% |
| Randomized controlled trials | 550 | 1.8% |
Method: PubMed query "Graft vs Host Disease"[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.
Xenopax for the treatment of steroid-refractory acute graft-versus-host disease: the RELAX study [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundSteroid-refractory (SR) acute graft-versus-host disease (aGVHD) is the major cause of early mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT).
- Closing excerpt
- ConclusionsOur real-world findings suggest that xenopax is an effective and safe treatment for SR-aGVHD.
- 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 (289 words)
BackgroundSteroid-refractory (SR) acute graft-versus-host disease (aGVHD) is the major cause of early mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Xenopax, a novel and the only available humanized interleukin-2 (IL-2) receptor antagonist, has been approved as a category 2 biological product by the National Medical Products Administration. This study aims to evaluate the efficacy, safety, and prognostic factors of xenopax treatment for SR-aGVHD in real-world settings.MethodsThis was a multicenter, retrospective analysis that included SR-aGVHD patients who received xenopax at 17 hospitals across China. The data were collected from the electronic medical records in transplant databases. The primary endpoint was the 28-day overall response rate (ORR), encompassing both partial and complete responses. This study also included independent historical SR-aGVHD cohorts treated with best available treatments (BATs, n = 1009) as controls.ResultsIn total, 172 SR-aGVHD patients were included in this study. Xenopax was administered either as monotherapy (n = 60) or in combination with other second-line treatments (n = 112). The ORR was 64.5% [95% confidence interval (CI) 57.3-71.7%] on day 28 and 82.6% (95% CI 76.9-88.3%) at any time after xenopax treatment. The 2-year probabilities of disease-free survival, overall survival, non-relapse mortality (NRM), and relapse after xenopax treatment were 57.0% (95% CI 49.9-65.0%), 68.0% (95% CI 61.4-75.4%), 24.2% (95% CI 18.0-30.9%), and 19.0% (95% CI 12.8-25.2%), respectively. The ORR and survival were similar between patients with and without prior second-line treatments. The conditioning regimen and human leukocyte antigen disparity did not impact the efficacy of xenopax treatment. According to the multivariate analysis, the presence of grade III-IV aGVHD did not adversely affect the therapeutic response or survival. Xenopax also showed some superiority over BATs in historical cohorts.ConclusionsOur real-world findings suggest that xenopax is an effective and safe treatment for SR-aGVHD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41024116 · DOI · PMC12477784
Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Bronchiolitis obliterans syndrome (BOS) is a progressive, fatal obstructive lung disease that occurs following lung transplant, where it is termed chronic lung allograft dysfunction BOS (CLAD-BOS), or as the primary manifestation of pulmonary chronic graft versus host disease (cGVHD-BOS) following allogeneic hematopoietic stem cell transplant.
- Closing excerpt
- These data suggest substantial cellular and molecular overlap between CLAD- and cGVHD-BOS and, therefore, common pathways for possible therapeutic intervention.
- 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 (182 words)
Bronchiolitis obliterans syndrome (BOS) is a progressive, fatal obstructive lung disease that occurs following lung transplant, where it is termed chronic lung allograft dysfunction BOS (CLAD-BOS), or as the primary manifestation of pulmonary chronic graft versus host disease (cGVHD-BOS) following allogeneic hematopoietic stem cell transplant. Disease pathogenesis is poorly understood; however, chronic alloreactivity is common to both conditions, suggesting a shared pathophysiology. We performed single-cell RNA-Seq (scRNA-Seq) on explanted human lungs from 4 patients with CLAD-BOS, 3 patients with cGVHD-BOS, and 3 deceased controls to identify cell types, genes, and pathways enriched in BOS to better understand disease mechanisms. In both forms of BOS, we found an expanded population of CD8+ tissue resident memory T cells (TRM), which was distinct to BOS compared with other chronic lung diseases. In addition, BOS samples expressed genes and pathways associated with macrophage chemotaxis and proliferation, including in nonimmune cell populations. We also identified dysfunctional stromal cells in BOS, characterized by pro- and antifibrotic gene programs. These data suggest substantial cellular and molecular overlap between CLAD- and cGVHD-BOS and, therefore, common pathways for possible therapeutic intervention.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40232854 · DOI · PMC12128974
Acetyl-CoA carboxylase 1 inhibition increases Treg metabolism and graft-versus-host disease treatment efficacy via mitochondrial fusion [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Tregs are critical for maintaining immune homeostasis, and their adoptive transfer can treat murine inflammatory disorders.
- Closing excerpt
- Together, these data suggest that ACC1 manipulation may be exploited to modulate Treg function in patients.
- 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 (200 words)
Tregs are critical for maintaining immune homeostasis, and their adoptive transfer can treat murine inflammatory disorders. In patients, Treg therapies have been variably efficacious. Therefore, new strategies to enhance Treg therapeutic efficacy are needed. Tregs predominantly depend on oxidative phosphorylation (OXPHOS) for energy and suppressive function. Fatty acid oxidation (FAO) contributes to Treg OXPHOS and can be important for Treg "effector" differentiation, but FAO activity is inhibited by coordinated activity of the isoenzymes acetyl-CoA carboxylase-1 and -2 (ACC1 and ACC2). Here, we show that small-molecule inhibition or Treg-specific genetic deletion of ACC1 significantly increases Treg suppressive function in vitro and in mice with established chronic graft-versus-host disease. ACC1 inhibition skewed Tregs toward an "effector" phenotype and enhanced FAO-mediated OXPHOS, mitochondrial function, and mitochondrial fusion. Inhibiting mitochondrial fusion diminished the effect of ACC1 inhibition. Reciprocally, promoting mitochondrial fusion, even in the absence of ACC1 modulation, resulted in a Treg functional and metabolic phenotype similar to that seen with ACC1 inhibition, indicating a key role for mitochondrial fusion in Treg-suppressive potency. Ex vivo-expanded, ACC1 inhibitor-treated human Tregs similarly augmented suppressor function, as observed with murine Tregs. Together, these data suggest that ACC1 manipulation may be exploited to modulate Treg function in patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41026528 · DOI · PMC12646659
The BIOPREVENT machine-learning algorithm predicts chronic graft-versus-host disease and mortality risk using posttransplant biomarkers [4]
Abstract reading summary — source excerpts
- Opening excerpt
- BACKGROUNDChronic graft-versus-host disease (cGVHD) is a major contributor to nonrelapse mortality (NRM) following hematopoietic cell transplantation (HCT).
- Closing excerpt
- FUNDINGR01CA264921, U10HL069294, U24HL138660, R01HD074587, and P01HL158505.
- 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 (249 words)
BACKGROUNDChronic graft-versus-host disease (cGVHD) is a major contributor to nonrelapse mortality (NRM) following hematopoietic cell transplantation (HCT). Whether machine-learning (ML) models with biomarkers improve the accuracy for predicting future cGVHD/NRM is not established.METHODSWe developed BIOPREVENT (BIOmarkers PREVENTion), a ML algorithm using data from 1,310 HCT recipients, incorporating 7 plasma proteins measured at Day 90/100 post-HCT and 9 clinical variables. Patients were divided into training and validation datasets. ML models - including CoxXGBoost, Group SCAD, Adaptive Group Lasso, Random Survival Forests, and Bayesian Additive Regression Trees (BART) - were used to estimate time-varying Area Under the ROC Curve (AUCt) at Days 180, 270, 360, and 540. Deep learning models were also evaluated.RESULTSML models with biomarkers outperformed clinical-only models for predicting cGVHD, with BART and CoxXGBoost achieving AUCt greater than 0.65 at 1 year. For NRM, models with biomarkers achieved AUCt ranging from 0.75-0.91. Deep learning did not outperform other ML approaches. BART consistently demonstrated high predictive accuracy and was selected for the final BIOPREVENT model. Calibration curves aligned with observed values. Variable importance analysis identified MMP3 and CXCL9 as key for cGVHD prediction and IL1RL1 and sCD163 for NRM. Cumulative incidences of cGVHD and NRM differed significantly based on BIOPREVENT-defined cutpoints.CONCLUSIONBIOPREVENT accurately predicts individual risk of future cGVHD and NRM using biomarkers at 3 months post-HCT. A publicly available R Shiny web application supports its clinical use. Further studies are needed to explore its role in guiding preemptive therapy.TRIAL REGISTRATIONBMTCTN 0201, BMTCTN 1202, and NCT02194439.FUNDINGR01CA264921, U10HL069294, U24HL138660, R01HD074587, and P01HL158505.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41697751 · DOI · PMC12904722
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 Prophylaxis and management of graft-versus-host disease after stem-cell transplantation for haematological malignancies: updated consensus recommendations of the European Society for Blood and Marrow Transplantation [5]
- Research article Deep insight into cytokine storm: from pathogenesis to treatment [6]
- Research article Efficacy and safety of transcutaneous electrical nerve stimulation (TENS) for acute and chronic pain in adults: a systematic review and meta-analysis of 381 studies (the meta-TENS study) [7]
- Research article Survival after mesenchymal stromal cell therapy in steroid-refractory acute graft-versus-host disease: systematic review and meta-analysis [8]
- Research article Current perspectives on mesenchymal stromal cell therapy for graft versus host disease [9]
- Research article Mesenchymal stromal cells as treatment or prophylaxis for acute or chronic graft-versus-host disease in haematopoietic stem cell transplant (HSCT) recipients with a haematological condition [10]
References
- Cao LQ, Huo WX, Jiang EL, Fu YW, Xu XJ, Lei PC, et al.. Xenopax for the treatment of steroid-refractory acute graft-versus-host disease: the RELAX study. . 2025. PMID 41024116 · DOI · PMC12477784
- Mellors PW, Lange AN, Casino Remondo B, Shestov M, Planer JD, Peterson AR, et al.. Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome. . 2025. PMID 40232854 · DOI · PMC12128974
- McDonald-Hyman C, Aguilar EG, Compeer EB, Zaiken MC, Rhee SY, Mohamed FA, et al.. Acetyl-CoA carboxylase 1 inhibition increases Treg metabolism and graft-versus-host disease treatment efficacy via mitochondrial fusion. . 2025. PMID 41026528 · DOI · PMC12646659
- Martens MJ, Dutta D, Yu Y, Rein LE, Ritz J, Logan BR, et al.. The BIOPREVENT machine-learning algorithm predicts chronic graft-versus-host disease and mortality risk using posttransplant biomarkers. . 2026. PMID 41697751 · DOI · PMC12904722
- Penack O, Marchetti M, Aljurf M, Arat M, Bonifazi F, Duarte RF, et al.. Prophylaxis and management of graft-versus-host disease after stem-cell transplantation for haematological malignancies: updated consensus recommendations of the European Society for Blood and Marrow Transplantation. Lancet Haematol. 2024. PMID 38184001 · DOI
- Nie J, Zhou L, Tian W, Liu X, Yang L, Yang X, et al.. Deep insight into cytokine storm: from pathogenesis to treatment. Signal Transduct Target Ther. 2025. PMID 40234407 · DOI · PMC12000524
- Johnson MI, Paley CA, Jones G, Mulvey MR, Wittkopf PG. Efficacy and safety of transcutaneous electrical nerve stimulation (TENS) for acute and chronic pain in adults: a systematic review and meta-analysis of 381 studies (the meta-TENS study). BMJ Open. 2022. PMID 35144946 · DOI · PMC8845179
- Hashmi S, Ahmed M, Murad MH, Litzow MR, Adams RH, Ball LM, et al.. Survival after mesenchymal stromal cell therapy in steroid-refractory acute graft-versus-host disease: systematic review and meta-analysis. Lancet Haematol. 2016. PMID 26765648 · DOI
- Kadri N, Amu S, Iacobaeus E, Boberg E, Le Blanc K. Current perspectives on mesenchymal stromal cell therapy for graft versus host disease. Cell Mol Immunol. 2023. PMID 37165014 · DOI · PMC10229573
- Fisher SA, Cutler A, Doree C, Brunskill SJ, Stanworth SJ, Navarrete C, et al.. Mesenchymal stromal cells as treatment or prophylaxis for acute or chronic graft-versus-host disease in haematopoietic stem cell transplant (HSCT) recipients with a haematological condition. Cochrane Database Syst Rev. 2019. PMID 30697701 · DOI · PMC6353308
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.