{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Quiniou G"],"funding":["Agence Nationale de la Recherche","Laboratoire d’Excellence Ecofect","Fondation pour la Recherche Médicale"],"pagination":["1837-1853"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11262231"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(8)"],"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"],"journal":["Autophagy"],"pubmed_title":["Impaired reprogramming of the autophagy flux in maturing dendritic cells from crohn disease patients with core autophagy gene-related polymorphisms."],"pmcid":["PMC11262231"],"funding_grant_id":["ANR-11-LABX-0042","ANR-22-CE17-0054-02","DEQ20170336729"],"pubmed_authors":["Nancey S","Quiniou G","Cervantes O","Dinet O","Rozieres A","Meunier C","Faure M","Duclaux-Loras R","Viret C","Boschetti G","Andromaque L","Verdet M"],"additional_accession":[]},"is_claimable":false,"name":"Impaired reprogramming of the autophagy flux in maturing dendritic cells from crohn disease patients with core autophagy gene-related polymorphisms.","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","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-06-02T04:29:59.64Z","creation":"2026-04-14T03:13:05.054Z"},"accession":"S-EPMC11262231","cross_references":{"pubmed":["38615686"],"doi":["10.1080/15548627.2024.2338574"]}}