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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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