Fiche publication
Date publication
février 2025
Journal
The Journal of cell biology
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAHRAM Siamak
,
Dr CARAPITO Raphaël
,
Dr GROS Frédéric
,
Dr MUELLER Christopher
,
Dr FLACHER Vincent
Tous les auteurs :
Arbogast F, Sal-Carro R, Boufenghour W, Frenger Q, Bouis D, Filippi De La Palavesa L, Fauny JD, Griso O, Puccio H, Fima R, Huby T, Gautier EL, Molitor A, Carapito R, Bahram S, Romani N, Clausen BE, Voisin B, Mueller CG, Gros F, Flacher V
Lien Pubmed
Résumé
Macroautophagy (often-named autophagy), a catabolic process involving autophagy-related (Atg) genes, prevents the accumulation of harmful cytoplasmic components and mobilizes energy reserves in long-lived and self-renewing cells. Autophagy deficiency affects antigen presentation in conventional dendritic cells (DCs) without impacting their survival. However, previous studies did not address epidermal Langerhans cells (LCs). Here, we demonstrate that deletion of either Atg5 or Atg7 in LCs leads to their gradual depletion. ATG5-deficient LCs showed metabolic dysregulation and accumulated neutral lipids. Despite increased mitochondrial respiratory capacity, they were unable to process lipids, eventually leading them to ferroptosis. Finally, metabolically impaired LCs upregulated proinflammatory transcripts and showed decreased expression of neuronal interaction receptors. Altogether, autophagy represents a critical regulator of lipid storage and metabolism in LCs, allowing their maintenance in the epidermis.
Mots clés
Langerhans Cells, metabolism, Autophagy, Animals, Lipid Metabolism, Epidermis, metabolism, Autophagy-Related Protein 7, genetics, Autophagy-Related Protein 5, metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondria, metabolism
Référence
J Cell Biol. 2025 02 3;224(2):
