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Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Dendritic cells (DCs) are central regulators of immune tolerance, and disturbances in their phenotype and function contribute to the breakdown of self-tolerance in systemic lupus erythematosus (SLE). Tolerogenic DCs (tolDCs), which suppress autoreactive responses and promote peripheral tolerance, are a promising therapeutic focus in autoimmune diseases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Here, we analyzed the transcriptional profiles of\n                      <jats:italic>in vitro<\/jats:italic>\n                      generated DCs derived from monocytes of individuals with SLE and healthy controls to identify disease-specific disruptions in tolerance associated pathways.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Interferon stimulated genes (ISGs) emerged as dominant markers across all cellular contexts, with monocytes exhibiting the most substantial enrichment; key ISGs (I\n                      <jats:italic>FI27, IFI44L, USP18, IFI6<\/jats:italic>\n                      ) acted as central hubs in regulatory networks, underscoring their diagnostic and pathogenic significance. In tolDCs from SLE donors, lipid metabolism pathways were selectively altered, suggesting impaired synthesis of pro-resolving lipid mediators. Additionally, diminished\n                      <jats:italic>IL10RA<\/jats:italic>\n                      expression and dysregulated\n                      <jats:italic>IRF4<\/jats:italic>\n                      activity in SLE moDCs indicated intrinsic defects in IL-10 mediated tolerogenic differentiation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Together, these findings suggest that interferon driven transcriptional rewiring, impaired IL-10 signaling, and aberrant lipid metabolic programming converge to compromise DCs tolerogenic capacity in SLE. This highlights key mechanistic pathways that could be targeted to restore immune tolerance and reduce chronic inflammation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1771959","type":"journal-article","created":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T09:12:47Z","timestamp":1780391567000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Gene expression profiling of dendritic cell tolerance dysfunction in women with systemic lupus erythematosus"],"prefix":"10.3389","volume":"17","author":[{"given":"Ana Laura","family":"Hern\u00e1ndez-Ledesma","sequence":"first","affiliation":[{"name":"Laboratorio Internacional de Investigaci\u00f3n sobre el Genoma Humano, Universidad Nacional Aut\u00f3noma de M\u00e9xico","place":["Santiago de Quer\u00e9taro, Mexico"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evelia 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