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.

免疫细胞激活特定的代谢程序以发挥其功能作用，包括适应其微环境。B1 B 细胞是组织驻留的、先天样 B 细胞。它们具有许多不同的特性，例如自我更新的能力和对有限的表位库快速反应的能力。支持这些功能的代谢途径尚不清楚。我们表明 B1 B 细胞在生物能量上比 B2 B 细胞更活跃，具有更高的糖酵解和氧化磷酸化率，并且依赖于糖酵解。它们获取外源脂肪酸并以液滴形式储存脂质。自噬在 B1a B 细胞中被差异激活，并且自噬基因Atg7的缺失导致由于自我更新失败而导致 B1a B 细胞的选择性损失。自噬缺陷型 B1a B 细胞下调关键代谢基因并积累功能失调的线粒体。因此，B1 B 细胞已经进化出一种独特的新陈代谢，以适应它们的驻留和特定的功能特性。