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The formation of long-lived immune memory cells specific for pathogens is critical for the establishment of long-term immune protection against future infections. BNIP3L/NIX and BNIP3, two functionally redundant BCL2 family members required for mitophagy, undergo significant upregulation after memory B cells are formed. Deletion of  Bnip3l  and  Bnip3  leads to mitochondrial accumulation, and increases in oxidative phosphorylation and fatty acid synthesis, resulting in the loss of memory B cells. These observations suggest that after the formation of memory B cells, mitophagy is critical for clearing superfluous mitochondria to re-shape the metabolic programs, thereby protecting the metabolic quiescence and longevity of memory B cells .

Regulation of Mitochondrial Homeostasis and Metabolic Programming in Memory B cells by Mitophagy