{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T07:01:50Z","timestamp":1790146910576,"version":"4.0.1"},"reference-count":56,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T00:00:00Z","timestamp":1790121600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Selpercatinib is a highly selective rearranged during transfection (RET) receptor tyrosine kinase inhibitor approved for RET fusion-positive cancers and known to penetrate the blood\u2013brain barrier. Although RET signaling has been implicated in neural development and cell survival, its role in microglia-mediated neuroinflammation and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation remains poorly understood. This study investigated whether Selpercatinib attenuates neuroinflammatory signaling in microglia by modulating RET-dependent kinase cascades.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Neuroinflammation was induced in BV2 microglial cells using lipopolysaccharide (LPS; 200 ng\/mL), followed by post-treatment with Selpercatinib (5 \u03bcM). For\n                      <jats:italic>in vivo<\/jats:italic>\n                      validation, male C57BL\/6N mice received systemic LPS administration (10 mg\/kg, i.p.) followed by Selpercatinib treatment (10 mg\/kg, i.p.), and hippocampal tissues were collected for analysis. Proinflammatory gene expression, RET-associated signaling pathways, microglial phenotypic markers, and NLRP3 inflammasome components were assessed using quantitative real-time polymerase chain reaction, western blotting, enzyme-linked immunosorbent assay, immunocytochemistry, and flow cytometry. RET-targeting siRNA was used to genetically validate the involvement of RET in LPS-induced inflammatory signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Selpercatinib reduced RET phosphorylation at Tyr1062 in LPS-stimulated BV2 microglia and reduced the mRNA expression of proinflammatory mediators, including\n                      <jats:italic>il-1\u03b2, il-6, tnf-\u03b1, cox-2<\/jats:italic>\n                      ,\n                      <jats:italic>inos, ccl-2<\/jats:italic>\n                      , and\n                      <jats:italic>ccl-7<\/jats:italic>\n                      in BV2 microglia. Mechanistically, Selpercatinib attenuated AKT and ERK phosphorylation, inhibited NF-\u03baB nuclear translocation, and reduced CREB phosphorylation. Similarly, RET knockdown reduced LPS-induced proinflammatory gene expression and attenuated AKT\/ERK\u2013NF-\u03baB\/CREB signaling, providing genetic evidence for the involvement of RET in these inflammatory responses. Selpercatinib also modulated LPS-induced microglial activation by decreasing the expression of reactive microglial markers, including CD16\/32, disease-associated microglia-associated Clec7a, and microglial neurodegenerative phenotype-associated Galectin-3, while increasing CD206, the marker associated with tissue repair. In addition, Selpercatinib significantly reduced LPS-induced intracellular ROS generation. Furthermore, Selpercatinib inhibited NLRP3 inflammasome activation, as evidenced by reduced levels of NLRP3, ASC, pro-caspase-1, cleaved caspase-1, GSDMD, and IL-1\u03b2 in BV2 microglia. Consistent with the\n                      <jats:italic>in vitro<\/jats:italic>\n                      findings, Selpercatinib attenuated LPS-induced hippocampal\n                      <jats:italic>il-1\u03b2<\/jats:italic>\n                      gene expression\n                      <jats:italic>in vivo<\/jats:italic>\n                      and reduced NLRP3 inflammasome-related proteins, including ASC, pro-caspase-1, cleaved caspase-1 and GSDMD-F and N in the hippocampus of mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Selpercatinib attenuated the development of microglia-mediated neuroinflammatory responses through modulation of RET-associated AKT\/ERK\u2013NF-\u03baB\/CREB signaling and suppression of NLRP3 inflammasome activation. These findings provide a mechanistic basis for further investigating Selpercatinib as an early intervention agent for neuroinflammatory responses.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1899666","type":"journal-article","created":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T06:20:21Z","timestamp":1790144421000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Selpercatinib mitigates microglia-mediated neuroinflammation by inhibiting RET signaling and NLRP3 inflammasome activation"],"prefix":"10.3389","volume":"17","author":[{"given":"Jung Ki","family":"Min","sequence":"first","affiliation":[{"name":"Multidimensional Genomics Research Center, Kangwon National University","place":["Chuncheon, Republic of Korea"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daeun","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Bio-Health 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