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Omics · dataset · 2026

Supplementary file 1_Myeloid EGR1 contributes to Th17/Treg imbalance during acute liver allograft rejection in a rat model.docx

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Background<p>Ischemia-reperfusion injury (IRI) and acute rejection (AR) limit liver transplantation success.

Description

Early growth response 1 (EGR1) mediates stress and inflammation, yet its cellular distribution and potential involvement in adaptive alloimmunity during distinct post-transplant stages remain unclear.</p>Methods<p>A rat orthotopic liver transplantation model was used to evaluate graft injury and EGR1 spatiotemporal expression during IRI (6–24 h) and AR (5–10 d).

Public scRNA-seq data and virtual knockout analysis were used to assess the cellular distribution and potential regulatory role of Egr1. EGR1-overexpressing bone marrow-derived dendritic cells (BMDCs) were co-cultured with CD4<sup>+</sup> T-cells to assess cytokine secretion, proliferation, and shifted Th17/Treg differentiation.</p>Results<p>Both syngeneic and allogeneic grafts exhibited early IRI. By days 5–10, allografts developed AR with elevated liver enzymes and Banff scores.

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EGR1 rose transiently during IRI but re-escalated exclusively in allografts during AR, localizing to portal infiltrates. scRNA-seq showed preferential Egr1 expression in graft myeloid cells, while virtual knockout suggested immune-related regulatory effects. EGR1-associated APC activation and Th17-associated responses were observed in rejecting allografts. EGR1 overexpression in BMDCs promoted pro-inflammatory cytokine secretion, T-cell proliferation, and altered Th17/Treg-associated responses.</p>Conclusion<p>EGR1 contributes to liver allograft rejection by modulating myeloid APC responses and Th17/Treg-associated T-cell responses, highlighting its potential as a therapeutic target for AR.</p>

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Immunology 70%
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