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B1a B cells require autophagy for metabolic homeostasis and self-renewal

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Item Type:Article
Title:B1a B cells require autophagy for metabolic homeostasis and self-renewal
Creators Name:Clarke, A.J., Riffelmacher, T., Braas, D., Cornall, R.J. and Simon, A.K.
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 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.
Keywords:Autophagy, Autophagy-Related Protein 7, B-Lymphocyte Subsets, Cell Lineage, Cell Self Renewal, Cell Survival, Fatty Acids, Glycolysis, Homeostasis, Inbred C57BL Mice, Knockout Mice, Lipid Metabolism, Oxidative Phosphorylation, Animals, Mice
Source:Journal of Experimental Medicine
ISSN:0022-1007
Publisher:Rockefeller University Press
Volume:215
Number:2
Page Range:399-413
Date:5 February 2018
Official Publication:https://doi.org/10.1084/jem.20170771
PubMed:View item in PubMed

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