ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2019
Usefulness of gene expression profiling of bronchoalveolar lavage cells in acute lung allograft rejection.
Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 46 citations in OpenAlex.
- Bronchoalveolar lavage for supporting acute cellular rejection in lung transplant recipients: A retrospective analysis.JHLT open · 2026Article
- Immune gene correlation networks differentiate both chronic lung allograft dysfunction and survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Post-lung transplant surveillance in 2026: current practice, variability, and the need for standardization.Transplant international : official journal of the European Society for Organ Transplantation · 2026Review
- Development and validation of a bronchoalveolar lavage genomic classifier for acute cellular rejection.EBioMedicine · 2025Article
- BALF Lymphocyte and Cytokine Profiling as Biomarkers of Acute Rejection After Lung Transplantation.Journal of personalized medicine · 2025Article
- Transition from Transbronchial Forceps to Cryobiopsy After Lung Transplantation: A Single-Centre Experience.Life (Basel, Switzerland) · 2024Article
- Airway epithelium in lung transplantation: a potential actor for post-transplant complications?European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Macrophage and CD8 T cell discordance are associated with acute lung allograft dysfunction progression.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2024Article
- Leveraging blood-based transcriptomics to detect acute cellular rejection in lung transplant.JHLT open · 2024Article
- CD16American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023Article
- Screening gene signatures for clinical response subtypes of lung transplantation.Molecular genetics and genomics : MGG · 2022Article
- Transbronchial Cryobiopsy Compared to Forceps Biopsy for Diagnosis of Acute Cellular Rejection in Lung Transplants: Analysis of 63 Consecutive Procedures.Life (Basel, Switzerland) · 2022Article
- Inflammation on bronchoalveolar lavage cytology is associated with decreased chronic lung allograft dysfunction-free survival.Clinical transplantation · 2022Article
- Modulation of tissue resident memory T cells by glucocorticoids after acute cellular rejection in lung transplantation.The Journal of experimental medicine · 2022Article
- Molecular diagnostics for CLAD: When and where?American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- Lymphocytic Airway Inflammation in Lung Allografts.Frontiers in immunology · 2022Review
- Natural killer cell-related prognosis signature characterizes immune landscape and predicts prognosis of HNSCC.Frontiers in immunology · 2022Article
- Rapid molecular detection of airway pathogens in lung transplant recipients.Transplant infectious disease : an official journal of the Transplantation Society · 2021Observational
- Type-1 immunity and endogenous immune regulators predominate in the airway transcriptome during chronic lung allograft dysfunction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Article
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14 authors at 7 institutions in 2 countries.
Funding
Abstract
backgroundChronic lung allograft dysfunction (CLAD) is the main limitation to long-term survival after lung transplantation. Because effective therapies are lacking, early identification and mitigation of risk factors is a pragmatic approach to improve outcomes. Acute cellular rejection (ACR) is the most pervasive risk factor for CLAD, but diagnosis requires transbronchial biopsy, which carries risks. We hypothesized that gene expression in the bronchoalveolar lavage (BAL) cell pellet (CP) could replace biopsy and inform on mechanisms of CLAD.
methodsWe performed RNA sequencing on BAL CPs from 219 lung transplant recipients with A-grade ACR (n = 61), lymphocytic bronchiolitis (n = 58), infection (n = 41), or no rejection/infection (n = 59). Differential gene expression was based on absolute fold difference >2.0 and Benjamini-adjusted p-value ≤0.05. We used the Database for Annotation, Visualization and Integrated Discovery Bioinformatics Resource for pathway analyses. For classifier modeling, samples were randomly split into training (n = 154) and testing sets (n = 65). A logistic regression model using recursive feature elimination and 5-fold cross-validation was trained to optimize area under the curve (AUC).
resultsDifferential gene expression identified 72 genes. Enriched pathways included T-cell receptor signaling, natural killer cell-mediated cytotoxicity, and cytokine-cytokine receptor interaction. A 4-gene model (AUC = 0.72) and classification threshold defined in the training set exhibited fair performance in the testing set; accuracy was 76%, specificity 82%, and sensitivity 60%. In addition, classification as ACR was associated with worse CLAD-free survival (hazard ratio = 2.42; 95% confidence interval = 1.29-4.53).
conclusionsBAL CP gene expression during ACR is enriched for immune response pathways and shows promise as a diagnostic tool for ACR, especially ACR that is a precursor of CLAD.
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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.