<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Batliner M</submitter><funding>Deutsche Forschungsgemeinschaft (DFG)</funding><funding>Deutsche Forschungsgemeinschaft</funding><pagination>e0073224</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11323541</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(8)</volume><pubmed_abstract>&lt;i>Candida albicans,&lt;/i> an opportunistic fungal pathogen, produces the quorum-sensing molecule farnesol, which we have shown alters the transcriptional response and phenotype of human monocyte-derived dendritic cells (DCs), including their cytokine secretion and ability to prime T cells. This is partially dependent on the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ), which has numerous ligands, including the sphingolipid metabolite sphingosine 1-phosphate. Sphingolipids are a vital component of membranes that affect membrane protein arrangement and phagocytosis of &lt;i>C. albicans&lt;/i> by DCs. Thus, we quantified sphingolipid metabolites in monocytes differentiating into DCs by High-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Farneso</pubmed_abstract><journal>mBio</journal><pubmed_title>The &lt;i>Candida albicans&lt;/i> quorum-sensing molecule farnesol alters sphingolipid metabolism in human monocyte-derived dendritic cells.</pubmed_title><pmcid>PMC11323541</pmcid><funding_grant_id>417857878</funding_grant_id><funding_grant_id>492620490</funding_grant_id><funding_grant_id>210879364</funding_grant_id><pubmed_authors>Riedel A</pubmed_authors><pubmed_authors>Batliner M</pubmed_authors><pubmed_authors>Schempp R</pubmed_authors><pubmed_authors>Fekete A</pubmed_authors><pubmed_authors>Kohler T</pubmed_authors><pubmed_authors>Wigger D</pubmed_authors><pubmed_authors>Schumacher F</pubmed_authors><pubmed_authors>Fohmann I</pubmed_authors><pubmed_authors>Kurzai O</pubmed_authors><pubmed_authors>Prell A</pubmed_authors><pubmed_authors>Vaeth M</pubmed_authors><pubmed_authors>Kleuser B</pubmed_authors><pubmed_authors>Vivas W</pubmed_authors><pubmed_authors>Nieuwenhuizen NE</pubmed_authors></additional><is_claimable>false</is_claimable><name>The &lt;i>Candida albicans&lt;/i> quorum-sensing molecule farnesol alters sphingolipid metabolism in human monocyte-derived dendritic cells.</name><description>&lt;i>Candida albicans,&lt;/i> an opportunistic fungal pathogen, produces the quorum-sensing molecule farnesol, which we have shown alters the transcriptional response and phenotype of human monocyte-derived dendritic cells (DCs), including their cytokine secretion and ability to prime T cells. This is partially dependent on the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ), which has numerous ligands, including the sphingolipid metabolite sphingosine 1-phosphate. Sphingolipids are a vital component of membranes that affect membrane protein arrangement and phagocytosis of &lt;i>C. albicans&lt;/i> by DCs. Thus, we quantified sphingolipid metabolites in monocytes differentiating into DCs by High-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Farneso</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2025-04-19T20:39:22.825Z</modification><creation>2025-04-19T20:39:22.825Z</creation></dates><accession>S-EPMC11323541</accession><cross_references><pubmed>38953353</pubmed><doi>10.1128/mbio.00732-24</doi></cross_references></HashMap>