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Gene expression of wild-type and Nix-/-Bnip3-/- memory B cells

ABSTRACT: Memory B cells are long-lived lymphocytes essential for humoral immunological memory. Autophagy is required for the long-term survival of memory B cells, however, the molecular mechanisms for the protection by autophagy have not been fully elucidated. Here we show that mitochondrial autophagy mediated by Nix and Bnip3 prevents necroptosis in memory B cells by maintaining mitochondrial homeostasis and normal lipid metabolism. In mice with B cell-specific deletion of Nix and Bnip3, memory B cells showed significant increases in viable mitochondria and de novo fatty acid synthesis, with accumulation of lipid droplets in the cytoplasm and accelerated cell death. Inhibiting the mitochondrial citrate transporter Slc25a1 or silencing the necroptosis gene Ripk3 rescued Nix–/–Bnip3–/– memory B cells in vivo. These data indicate that Nix- and Bnip3-dependent mitochondrial autophagy in memory B cells is important for restricting de novo fatty acid synthesis and preventing necroptosis. Our results suggest a mechanism for autophagy in the maintenance of mitochondrial homeostasis for the protection of immunological memory.

ORGANISM(S): Mus musculus

PROVIDER: GSE176047 | GEO | 2021/06/03

REPOSITORIES: GEO

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Project description:This a model from the article: Evolution of immunological memory and the regulation of competition between pathogens. Wodarz D. Curr Biol 2003 Sep 16;13(18):1648-52 13678598 , Abstract: Memory is a central characteristic of immune responses. It is defined as an elevated number of specific immune cells that remain after resolution of infection and can protect the host against reinfection. The evolution of immunological memory is subject to debate. The advantages of memory discussed so far include protection from reinfection, control of chronic infection, and the transfer of immune function to the next generation. Mathematical models are used to identify a new force that can drive the evolution of immunological memory: the duration of memory can regulate the degree of competition between different pathogens. While a long duration of memory provides lasting protection against reinfection, it may also allow an inferior pathogen species to persist. This can be detrimental for the host if the inferior pathogen is more virulent. On the other hand, a shorter duration of memory ensures that an inferior pathogen species is excluded. This can be beneficial for the host if the inferior pathogen is more virulent. Thus, while in the absence of pathogen diversity memory is always expected to evolve to a long duration, under specific circumstances, memory can evolve toward shorter durations in the presence of pathogen diversity. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Wodarz D. (2003) - version=1.0 The original CellML model was created by: Catherine Lloyd c.lloyd@auckland.ac.nz The University of Auckland This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

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Gene expression of wild-type and Nix-/-Bnip3-/- memory B cells

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