J. Exp. Med. https://doi.org/10.1084/jem.20170771 (11 January 2018)
CD5+ B-1a cells function as a distinct subset of effector B cells. In The Journal of Experimental Medicine, Clarke et al. reveal that B-1a cells use a distinct metabolism that differs from that used by follicular B-2 cells. B-1a cells exhibit a higher rate of glycolysis, lipid uptake and fatty-acid synthesis than that of other B cell subsets and are more dependent on autophagy than are other B cell subsets. Notably, these cells are less flexible in their ability to alter their cellular metabolism, as inhibition of either glycolysis or autophagy induces the rapid death of B-1a cells. The latter scenario results in the hyperpolarization of mitochondria and probably increased oxidative stress within cells. Although this metabolism benefits rapid antibody production, it might explain why this B cell subset is restricted to lipid-rich niches.
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Dempsey, L.A. B-1a cell metabolism. Nat Immunol 19, 206 (2018). https://doi.org/10.1038/s41590-018-0060-z
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DOI: https://doi.org/10.1038/s41590-018-0060-z