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Sentinel flaps recapitulate key inflammatory aspects of human face transplant rejection

ABSTRACT: Sentinel flaps are used for remote-site monitoring in vascularized composite allotransplantation (VCA), but their molecular relationship to facial allografts during rejection has not been defined. We analyzed gene expression in formalin-fixed paraffin-embedded (FFPE) skin biopsies from facial allografts (FA) and sentinel flaps (SF) obtained from five face transplant recipients at Brigham and Women’s Hospital. Simultaneous 4-mm punch biopsies were collected from FA and SF sites during grade 0 (non-rejection) and grade 3 (acute rejection) episodes, yielding 14 matched pairs. RNA was extracted and profiled using the NanoString nCounter PanCancer Immune Profiling Panel (730 immune-related genes). Data were normalized to positive controls and housekeeping genes using NanoString nSolver v4.0. Differentially expressed genes were identified by comparing grade 3 versus grade 0 samples in FA and SF separately. These datasets provide transcriptional profiles of acute rejection in human face transplants and sentinel flaps for use in comparative and mechanistic studies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE313108 | GEO | 2025/12/10

REPOSITORIES: GEO

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Project description:CONTEXT Slowly progressive chronic tubulo-interstitial damage jeopardizes long-term renal allograft survival. Both immune and non-immune mechanisms are thought to contribute, but the most promising targets for timely intervention have not been identified. OBJECTIVE In the current study we seek to determine the driving force behind progressive histological damage of renal allografts, without the interference of donor pathology, delayed graft function and acute graft rejection. DESIGN We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. PATIENTS Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection. RESULTS In this highly cross-validated study, we demonstrate the significant association of established, ongoing and future chronic histological damage with regulation of adaptive immune gene expression (T-cell and B-cell transcript sets) and innate immune response gene expression (dendritic cell, NK-cell, mast cell and granulocyte transcripts). We demonstrate the ability of gene expression analysis to perform as a quantitative marker for ongoing inflammation with a wide dynamic range: from subtle subhistological inflammation prior to development of chronic damage, over moderate subclinical inflammation associated with chronic histological damage, to marked inflammation of Banff-grade acute T-cell mediated rejection. CONCLUSION Progressive chronic histological damage after kidney transplantation is associated with significant regulation of both innate and adaptive immune responses, months before the histological lesions appear. This study therefore corroborates the hypothesis that quantitative inflammation below the diagnostic threshold of classic T-cell or antibody-mediated rejection is associated with early subclinical stages of progressive renal allograft damage. We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection.

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Sentinel flaps recapitulate key inflammatory aspects of human face transplant rejection

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