Daughter B cells are not created equal

Following the binding of B cell receptors (BCR) to cognate antigens exposed on presenting cells, B cells rapidly spread over antigen-containing surface. During B cell spreading, antigen-BCR microclusters are continually assembled at the periphery of the contact area between the cells. The initial spreading response is followed by a contraction phase, which results in the accumulation of antigen-BCR complexes in the center of the mature immunological synapse. Recent evidence suggests that the centripetal movement of antigen-BCR complexes is mediated by the recruitment of the microtubule motor dynein to the signaling BCR microcluster. Trafficking of antigen-BCR complexes to the minus end of the underlying microtubule network may also explain how antigen-BCR complexes are extracted from mature immunological synapse and targeted to endosomes. Antigen internalisation in B cells indeed correlates with a dramatic reorganization of endosomal compartment, during which discrete scattered peripheral endosomes fuse to form a cluster of few large MHC II-enriched vesicles containing antigens (MIIC) that are concentrated in the vicinity of the microtubule organization center. Once established, antigen polarization is maintained in antigen-experienced B cells when they migrate to the B zone-T zone boundary. There, endosomal antigen stock allows for presentation of processed antigenic peptide in MHC II molecules to cognate CD4 T cells, which, in turn, provide costimulatory signals that trigger B cell division and differentiation. Optimal protection against pathogens indeed requires that following encounter of antigen, Daughter B cells are not created equal Asymmetric segregation of antigen during B cell division