<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhao P</submitter><funding>National Natural Science Foundation of China</funding><funding>Beijing Natural Science Foundation</funding><pagination>0895</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12454940</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8</volume><pubmed_abstract>T lymphocyte dysfunction represents a pivotal determinant of immunosuppression in sepsis. Our previous studies demonstrated that nuclear fragile X mental retardation-interacting protein 1 (NUFIP1)-mediated ribophagy conferred cytoprotection against apoptosis in CD4&lt;sup>+&lt;/sup> T lymphocytes during sepsis, thereby preserving host immunocompetence. Despite growing evidence linking PANoptosis to the pathogenesis of various diseases, the potential role of ribophagy in modulating CD4&lt;sup>+&lt;/sup> T lymphocytes' PANoptosis in sepsis remains largely unclear. In the present study, we employed both lipopolysaccharide-stimulated Jurkat T cells and cecal ligation and puncture (CLP)-induced sepsis models to demonstrate marked exacerbation of CD4&lt;sup>+&lt;/sup> T lymphocyte PANoptosis following &lt;i>NUFIP1&lt;/</pubmed_abstract><journal>Research (Washington, D.C.)</journal><pubmed_title>NUFIP1-Mediated Ribophagy Alleviates PANoptosis of CD4&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; T Lymphocytes in Sepsis via the cGAS-STING Pathway.</pubmed_title><pmcid>PMC12454940</pmcid><funding_grant_id>Nos. 82130062, 82241062, 82372158</funding_grant_id><funding_grant_id>7244296</funding_grant_id><pubmed_authors>Xia Y</pubmed_authors><pubmed_authors>Chen N</pubmed_authors><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Luo Z</pubmed_authors><pubmed_authors>Fu Z</pubmed_authors><pubmed_authors>Du X</pubmed_authors><pubmed_authors>Yao R</pubmed_authors><pubmed_authors>Dong N</pubmed_authors><pubmed_authors>He P</pubmed_authors><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Yao Y</pubmed_authors><pubmed_authors>Zhao P</pubmed_authors><pubmed_authors>Zheng L</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>NUFIP1-Mediated Ribophagy Alleviates PANoptosis of CD4&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; T Lymphocytes in Sepsis via the cGAS-STING Pathway.</name><description>T lymphocyte dysfunction represents a pivotal determinant of immunosuppression in sepsis. Our previous studies demonstrated that nuclear fragile X mental retardation-interacting protein 1 (NUFIP1)-mediated ribophagy conferred cytoprotection against apoptosis in CD4&lt;sup>+&lt;/sup> T lymphocytes during sepsis, thereby preserving host immunocompetence. Despite growing evidence linking PANoptosis to the pathogenesis of various diseases, the potential role of ribophagy in modulating CD4&lt;sup>+&lt;/sup> T lymphocytes' PANoptosis in sepsis remains largely unclear. In the present study, we employed both lipopolysaccharide-stimulated Jurkat T cells and cecal ligation and puncture (CLP)-induced sepsis models to demonstrate marked exacerbation of CD4&lt;sup>+&lt;/sup> T lymphocyte PANoptosis following &lt;i>NUFIP1&lt;/</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-05-31T03:11:39.628Z</modification><creation>2026-05-31T03:07:56.537Z</creation></dates><accession>S-EPMC12454940</accession><cross_references><pubmed>40995563</pubmed><doi>10.34133/research.0895</doi></cross_references></HashMap>