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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.
Marginal zone B cells differentiate into plasma cells rapidly in response to T-cell-independent antigens, but how they do so is not clear. Here the authors show TACI cooperates with TLR signalling to drive mTOR activity and subsequent class switching and plasmablast differentiation.
Risk of infection is high after stroke, but the causes are not clear. Here the authors implicate altered beta–adrenergic signalling after stroke that results in a reduction in IgM-mediated protection by marginal zone B cells.
The signaling receptor Notch is required for the generation of marginal zone B cells. Hammad and colleagues show that Notch signaling activates the kinase Taok3 and surface expression of the metalloproteinase ADAM10, which commits transitional B cells to the marginal zone B cell fate.
Marginal zone B cells are mostly characterized in the context of host defense against bacterial blood-borne pathogens. Here the authors show that TLR4 signaling in these cells requires Fcα/μR (CD351) and that they are a major source of IL-6 in a mouse model of sepsis.
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.