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Spatial transcriptomics of IRF7-dependent pathway in chronic lung allograft dysfunction

ABSTRACT: Chronic lung allograft dysfunction (CLAD) remains a major barrier to long-term survival after lung transplantation. This study investigates the role of the type I interferon master regulator IRF7 in virus-induced airway fibrogenesis. Using NanoString GeoMx digital spatial profiling, we performed whole transcriptome spatial analysis of human lung tissue from CLAD, non-CLAD transplant, and non-transplanted normal donor lungs to characterize the spatial gene expression landscape associated with IRF7-dependent fibrotic pathways.

ORGANISM(S): Homo sapiens

PROVIDER: GSE326968 | GEO | 2026/04/08

REPOSITORIES: GEO

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Spatial transcriptomics of IRF7-dependent pathway in chronic lung allograft dysfunction

Project description:Spatial transcriptomics of IRF7-dependent pathway in chronic lung allograft dysfunction

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Periostin Defines a Pathological Fibroblast Program Enriched in Restrictive Allograft Syndrome

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Project description:Chronic lung allograft dysfunction (CLAD) is the leading cause of death in lung transplant recipients. CLAD is characterized clinically by a persistent decline in pulmonary function and histologically by the development of airway centered fibrosis known as bronchiolitis obliterans. We performed single-cell sequencing and spatial transcriptomic analysis of explanted tissues from human lung recipients with CLAD and donor control lungs.

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Project description:Chronic lung allograft dysfunction (CLAD) limits the long term survival after lung transplantation. CLAD is diagnosed late on the decline in lung function, when any immuno-intervention is ineffective. Identification of early forerunners of CLAD is therefore essential to prevent the progression of the disease before irreversible damages to the allograft. We used large-scale gene expression profiling of whole blood cells to identify early biomarkers of Bronchiolitis Obliterans Syndrome (BOS), the main form of CLAD. Microarray experiments performed from 80 patients (40 stable (STA) and 40 BOS) identify 47 genes differentially expressed between STA and BOS recipients. An independent set of patients (13 STA, 11 BOS) was then used for external validation by qPCR. POU Class 2 Associating Factor 1 (POU2AF1), T-cell leukemia/lymphoma protein 1A (TCL1A) and B-cell lymphocyte kinase (BLK) genes were identified and validated as predictive markers of BOS more than 6 months before diagnosis with AUCs of 0.83, 0.77 and 0.78 respectively. These genes allow stratifying upon CLAD risk (log-rank test p<0.01) and could provide clinicians with new tools to improve follow-up and adapt treatment of patients likely to develop BOS.

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