<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Quiniou G</submitter><funding>Agence Nationale de la Recherche</funding><funding>Laboratoire d’Excellence Ecofect</funding><funding>Fondation pour la Recherche Médicale</funding><pagination>1837-1853</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11262231</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(8)</volume><pubmed_abstract>Crohn disease (CD) is an inflammatory bowel disease whose pathogenesis involves inappropriate immune responses toward gut microbiota on genetically predisposed backgrounds. Notably, CD is associated with single-nucleotide polymorphisms affecting several genes involved in macroautophagy/autophagy, the catabolic process that ensures the degradation and recycling of cytosolic components and microorganisms. In a clinical translation perspective, monitoring the autophagic activity of CD patients will require some knowledge on the intrinsic functional status of autophagy. Here, we focused on monocyte-derived dendritic cells (DCs) to characterize the intrinsic quantitative features of the autophagy flux. Starting with DCs from healthy donors, we documented a reprogramming of the steady state flux</pubmed_abstract><journal>Autophagy</journal><pubmed_title>Impaired reprogramming of the autophagy flux in maturing dendritic cells from crohn disease patients with core autophagy gene-related polymorphisms.</pubmed_title><pmcid>PMC11262231</pmcid><funding_grant_id>ANR-11-LABX-0042</funding_grant_id><funding_grant_id>ANR-22-CE17-0054-02</funding_grant_id><funding_grant_id>DEQ20170336729</funding_grant_id><pubmed_authors>Nancey S</pubmed_authors><pubmed_authors>Quiniou G</pubmed_authors><pubmed_authors>Cervantes O</pubmed_authors><pubmed_authors>Dinet O</pubmed_authors><pubmed_authors>Rozieres A</pubmed_authors><pubmed_authors>Meunier C</pubmed_authors><pubmed_authors>Faure M</pubmed_authors><pubmed_authors>Duclaux-Loras R</pubmed_authors><pubmed_authors>Viret C</pubmed_authors><pubmed_authors>Boschetti G</pubmed_authors><pubmed_authors>Andromaque L</pubmed_authors><pubmed_authors>Verdet M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impaired reprogramming of the autophagy flux in maturing dendritic cells from crohn disease patients with core autophagy gene-related polymorphisms.</name><description>Crohn disease (CD) is an inflammatory bowel disease whose pathogenesis involves inappropriate immune responses toward gut microbiota on genetically predisposed backgrounds. Notably, CD is associated with single-nucleotide polymorphisms affecting several genes involved in macroautophagy/autophagy, the catabolic process that ensures the degradation and recycling of cytosolic components and microorganisms. In a clinical translation perspective, monitoring the autophagic activity of CD patients will require some knowledge on the intrinsic functional status of autophagy. Here, we focused on monocyte-derived dendritic cells (DCs) to characterize the intrinsic quantitative features of the autophagy flux. Starting with DCs from healthy donors, we documented a reprogramming of the steady state flux</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2026-06-02T04:29:59.64Z</modification><creation>2026-04-14T03:13:05.054Z</creation></dates><accession>S-EPMC11262231</accession><cross_references><pubmed>38615686</pubmed><doi>10.1080/15548627.2024.2338574</doi></cross_references></HashMap>