<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tu Q</submitter><funding>National Natural Science Foundation of China</funding><pagination>e13328</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9715356</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>55(12)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Mitochondrial DNA (mtDNA) is a potent activator for pro-inflammatory response. Dendritic cells (DCs) are immunosuppressed in sepsis, whether mtDNA mediates immunoparalysis in sepsis remains unknown.&lt;h4>Methods&lt;/h4>The mRNAs were assessed by qPCR. Flow cytometry was used to measure the expression of costimulatory molecules and the proliferation of CD4&lt;sup>+&lt;/sup> T cells. Western blot and immunofluorescence staining were used to analyse the expression of proteins. Cytokine secretion was detected by ELISA. Histology of lung tissue was used to assess the inflammatory injury.&lt;h4>Results&lt;/h4>Lipopolysaccharide-induced endotoxemia increased plasma mtDNA levels and immunoparalysis of spleen DCs, while hydrolysing mtDNA reversed immunoparalysis of spleen DCs in vivo. Moreover, c</pubmed_abstract><journal>Cell proliferation</journal><pubmed_title>Mitochondrial DNA mediates immunoparalysis of dendritic cells in sepsis via STING signalling.</pubmed_title><pmcid>PMC9715356</pmcid><funding_grant_id>81701943</funding_grant_id><funding_grant_id>81971813</funding_grant_id><pubmed_authors>Yao L</pubmed_authors><pubmed_authors>Zou Y</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Guo L</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Tu Q</pubmed_authors><pubmed_authors>Chen F</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Yuan Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mitochondrial DNA mediates immunoparalysis of dendritic cells in sepsis via STING signalling.</name><description>&lt;h4>Background&lt;/h4>Mitochondrial DNA (mtDNA) is a potent activator for pro-inflammatory response. Dendritic cells (DCs) are immunosuppressed in sepsis, whether mtDNA mediates immunoparalysis in sepsis remains unknown.&lt;h4>Methods&lt;/h4>The mRNAs were assessed by qPCR. Flow cytometry was used to measure the expression of costimulatory molecules and the proliferation of CD4&lt;sup>+&lt;/sup> T cells. Western blot and immunofluorescence staining were used to analyse the expression of proteins. Cytokine secretion was detected by ELISA. Histology of lung tissue was used to assess the inflammatory injury.&lt;h4>Results&lt;/h4>Lipopolysaccharide-induced endotoxemia increased plasma mtDNA levels and immunoparalysis of spleen DCs, while hydrolysing mtDNA reversed immunoparalysis of spleen DCs in vivo. Moreover, c</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-25T17:07:34.9Z</modification><creation>2025-04-06T05:02:14.116Z</creation></dates><accession>S-EPMC9715356</accession><cross_references><pubmed>36106559</pubmed><doi>10.1111/cpr.13328</doi></cross_references></HashMap>