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

View ORCID ProfileAlexander J Clarke, View ORCID ProfileThomas Riffelmacher, Daniel Braas, Richard J Cornall, View ORCID ProfileAnna Katharina Simon
doi: https://doi.org/10.1101/240523
Alexander J Clarke
1Kennedy Institute of Rheumatology and MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK
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  • For correspondence: alexander.clarke@kennedy.ox.ac.uk
Thomas Riffelmacher
1Kennedy Institute of Rheumatology and MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK
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Daniel Braas
3Department of Molecular and Medical Pharmacology, and UCLA Metabolomics Center UCLA, USA
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Richard J Cornall
2MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, Nuffield Department of Medicine, University of Oxford, Oxford, UK
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Anna Katharina Simon
1Kennedy Institute of Rheumatology and MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK
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Abstract

Specific metabolic programs are activated by immune cells to fulfil 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 due to a failure of self-renewal. Autophagy-deficient B1a B cells downregulate critical metabolic genes and accumulate dysfunctional mitochondria. B1 B cells therefore, have evolved a distinct metabolism adapted to their residence and specific functional properties.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted December 28, 2017.
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B1a B cells require autophagy for metabolic homeostasis and self-renewal
Alexander J Clarke, Thomas Riffelmacher, Daniel Braas, Richard J Cornall, Anna Katharina Simon
bioRxiv 240523; doi: https://doi.org/10.1101/240523
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B1a B cells require autophagy for metabolic homeostasis and self-renewal
Alexander J Clarke, Thomas Riffelmacher, Daniel Braas, Richard J Cornall, Anna Katharina Simon
bioRxiv 240523; doi: https://doi.org/10.1101/240523

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