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B1a B cells require autophagy for metabolic homeostasis and self-renewal.
Clarke, Alexander J; Riffelmacher, Thomas; Braas, Daniel; Cornall, Richard J; Simon, Anna Katharina.
  • Clarke AJ; Kennedy Institute of Rheumatology and Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK alexander.clarke@kennedy.ox.ac.uk.
  • Riffelmacher T; Kennedy Institute of Rheumatology and Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK.
  • Braas D; Department of Molecular and Medical Pharmacology and UCLA Metabolomics Center, University of California, Los Angeles, Los Angeles, CA.
  • Cornall RJ; Nuffield Department of Medicine, Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK.
  • Simon AK; Kennedy Institute of Rheumatology and Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK katja.simon@kennedy.ox.ac.uk.
J Exp Med ; 215(2): 399-413, 2018 02 05.
Article en En | MEDLINE | ID: mdl-29326381
ABSTRACT
Specific metabolic programs are activated by immune cells to fulfill their functional roles, which include adaptations to their microenvironment. B1 B cells are tissue-resident, innate-like B cells. They have many distinct properties, such as the capacity to self-renew and the ability to rapidly respond to a limited repertoire of epitopes. The metabolic pathways that support these functions are unknown. We show that B1 B cells are bioenergetically more active than B2 B cells, with higher rates of glycolysis and oxidative phosphorylation, and depend on glycolysis. They acquire exogenous fatty acids and store lipids in droplet form. Autophagy is differentially activated in B1a B cells, and deletion of the autophagy gene Atg7 leads to a selective loss of B1a B cells caused by a failure of self-renewal. Autophagy-deficient B1a B cells down-regulate critical metabolic genes and accumulate dysfunctional mitochondria. B1 B cells, therefore, have evolved a distinct metabolism adapted to their residence and specific functional properties.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Subgrupos de Linfocitos B Límite: Animals Idioma: En Año: 2018 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Subgrupos de Linfocitos B Límite: Animals Idioma: En Año: 2018 Tipo del documento: Article