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        <identifier>oai:figshare.com:article/33948925</identifier>
        <datestamp>2026-09-21T04:28:36Z</datestamp>
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          <dc:title>Supplementary file 1_Myeloid EGR1 contributes to Th17/Treg imbalance during acute liver allograft rejection in a rat model.docx</dc:title>
          <dc:creator>Yaming Ding (25079836)</dc:creator>
          <dc:creator>Jie Wang (16762)</dc:creator>
          <dc:creator>Shulin Li (222450)</dc:creator>
          <dc:creator>Guoxiang Shen (2102542)</dc:creator>
          <dc:creator>Lihong Chen (12138)</dc:creator>
          <dc:subject>Genetic Immunology</dc:subject>
          <dc:subject>acute rejection (AR)</dc:subject>
          <dc:subject>early growth response protein 1 (EGR1)</dc:subject>
          <dc:subject>liver transplantation</dc:subject>
          <dc:subject>myeloid cells</dc:subject>
          <dc:subject>single-cell RNA sequencing</dc:subject>
          <dc:subject>Th17/Treg balance</dc:subject>
          <dc:description>Background&lt;p&gt;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.&lt;/p&gt;Methods&lt;p&gt;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&lt;sup&gt;+&lt;/sup&gt; T-cells to assess cytokine secretion, proliferation, and shifted Th17/Treg differentiation.&lt;/p&gt;Results&lt;p&gt;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 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.&lt;/p&gt;Conclusion&lt;p&gt;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.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-21T04:28:36Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fimmu.2026.1901189.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Supplementary_file_1_Myeloid_EGR1_contributes_to_Th17_Treg_imbalance_during_acute_liver_allograft_rejection_in_a_rat_model_docx/33948925</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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