Protection of Quiescence and Longevity of IgG Memory B Cells by Mitochondrial Autophagy.

ABSTRACT: The development of long-lived immune memory cells against pathogens is critical for the success of vaccines to establish protection against future infections. However, the mechanisms governing the long-term survival of immune memory cells remain to be elucidated. In this article, we show that the maintenance mitochondrial homeostasis by autophagy is critical for restricting metabolic functions to protect IgG memory B cell survival. Knockout of mitochondrial autophagy genes, Nix and Bnip3, leads to mitochondrial accumulation and increases in oxidative phosphorylation and fatty acid synthesis, resulting in the loss of IgG⁺ memory B cells in mice. Inhibiting fatty acid synthesis or silencing necroptosis gene Ripk3 rescued Nix^-/-Bnip3^-/- IgG memory B cells, ind

SUBMITTER: Kodali S 

PROVIDER: S-EPMC8887795 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature