ArticleFrontiers in immunology2026
Myeloid EGR1 contributes to Th17/Treg imbalance during acute liver allograft rejection in a rat model.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Ischemia-reperfusion injury (IRI) and acute rejection (AR) limit liver transplantation success. 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. Methods: 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 Results: Both syngeneic and allogeneic grafts exhibited early IRI. By days 5-10, allografts developed AR with elevated liver enzymes and Banff scores. EGR1 rose transiently during IRI but re-escalated exclusively in allografts during AR, localizing to portal infiltrates. scRNA-seq showed preferential Conclusion: 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.
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