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Marginal zone B cells are a specialized population of B cells that are located in the marginal zone of the spleen. They secrete antibodies that help to protect against blood-borne viruses and bacteria.
Sustained exogenous Notch2 signaling prompts Follicular B cells to trans-differentiate into Marginal Zone B cells. This study reveals that under physiological conditions, Notch2 signalling regulates a fate choice in antigen activated Follicular B cells, dictating whether they develop into Germinal Center B cells or Marginal Zone B cells.
Cyster and colleagues show that CD97–CD55 interactions, which trigger Gα13–ARHGEF–Rho cytoskeletal signaling, are needed for proper MZ B cell positioning/retention in the spleen and for optimal antibody responses to T cell-independent antigens.
B cells pursue specific genetic programs to facilitate downstream cellular functions. Here the authors identify, using a combination of proteomic, transcriptomic and functional analyses, a group of mRNAs related to early activation and antibody production that are expressed in B cells without corresponding proteins, hinting a ‘poised’ state of B cells.
Follicular and marginal zone B (FoB and MZB, respectively) cells have divergent metabolic characteristics. Here the authors show that deficiency of glutamate cysteine ligase (Gclc), the enzyme for glutathione synthesis, differentially impacts FoB and MZB homeostasis, while specifically impeding FoB activation and downstream antiviral immunity.
Notch signalling is central to marginal zone B cell development, but it is unclear what path this development takes in vivo. Here the authors use a mouse that lacks these cells to show that transgenic induction of Notch2 is sufficient for development of marginal zone B cells via transdifferentiation from follicular B cells and that this mechanism can occur in wildtype mice.
Cellular metabolic screening identifies hyper-respiration, induced by gain-of-function mutations in the gene encoding succinate dehydrogenase, as a disease-driving immunometabolic trait of B cells from patients with primary antibody deficiency.
RNA-binding proteins (RBPs) take control of binary cell-fate 'decisions' and cellular identity in lymphoid organs, as the RBP ZFP36L1 is shown to negatively regulate the stability of the transcription factors KLF2 and IRF8 to control the maintenance, survival and localization of marginal zone B cells.
Small, soluble, ubiquitous ligands are difficult to visualize. Schwab and colleagues have created a functional receptor reporter that gauges the in vivo concentration, location and biological action of sphingolipids.
Innate lymphoid cells, marginal reticular cells and B cell–helper neutrophils interact to promote antibody secretion by B cells in the marginal zone of the spleen in humans and mice.