| First Author | Clarke AJ | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 2 | Pages | 399-413 |
| PubMed ID | 29326381 | Mgi Jnum | J:257686 |
| Mgi Id | MGI:6120025 | Doi | 10.1084/jem.20170771 |
| Citation | Clarke AJ, et al. (2018) B1a B cells require autophagy for metabolic homeostasis and self-renewal. J Exp Med 215(2):399-413 |
| abstractText | 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. |
