ArticleJournal of translational autoimmunity2026
A novel epigenetic regulation of JAM-A by EZH2-DNMT3A cascade contributes to T cell adhesion via the activation of Rap1a in lupus patients.
Article in Journal of translational autoimmunity, 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
Objectives: The peripheral blood T cells epigenetic modification and adhesion capacity alterations are the characteristic of SLE. EZH2 induces proinflammatory epigenetic changes in immune regulation. JAM-A widely involves in cell adhesion. However, the molecular regulation mechanisms between EZH2 and JAM-A in T cells of SLE patients remain undefined. Methods: EZH2 and JAM-A expression levels in T cells from SLE patients and healthy controls were evaluated via FCM and RT-qPCR. The regulatory mechanism between miR-26a-5p/EZH2 and JAM-A were investigated via BSP-PCR, ChIP assays, cell adhesion assays Results: We found the expression of EZH2 and JAM-A was upregulated in SLE patients' T cells. Mechanistically, EZH2 epigenetically repressed its target gene DNMT3A, mediated by H3K27me3, which consequently decreased the methylation levels in JAM-A promoter region, resulting in promoting the expression of JAM-A. Subsequently, JAM-A promoted the expression of its functionally relevant target gene Rap1a, a regulator of β1-integrin, involved in T cell adhesion. In addition, we show that both EZH2 and Rap1a are the target genes of miR-26a-5p. Specially, EZH2-mediated H3K27me3 modification in miR-26a-5p promoter region further inhibited the transcription of miR-26a-5p, resulting in the upregulation of EZH2 in T cells of SLE patients, creating a vicious cycle. And intraperitoneal administrating the inhibitor of EZH2 with GSK126 significantly ameliorated the nephritis in MRL/ Conclusion: This research reveals a novel epigenetic regulation of JAM-A by EZH2-DNMT3A cascade contributes to T cell adhesion capacity via the activation of Rap1a/β1-integrin in lupus patients.
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