Marginal zone 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.

Antibody production in plasma cells involves the unfold protein response (UPR), but how this is regulated is not clear. Here the authors show that mTORC1 signalling but not Xbp1-mediated transcription regulation in activated B cells is important for the induction of a UPR-related transcriptome that precedes full plasma cell functions.

Marginal zone B (MZB) cells shuttle between the marginal zone and lymphoid follicle to capture and present peripheral blood antigens. Here the authors show that shear force, such as blood flow from the sinus around the follicle, is a directional cue that induces MZB migration on ICAM-1, and that S1P signaling inhibits this directional migration.

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.