title: The NIK of time for B cells.
abstract: NF-κB-inducing kinase (NIK) is a key mediator of the noncanonical NF-κB signaling pathway, which is critical for B-cell development and function. Although complete deletion of NIK in mice has been shown to result in defective B cells and impaired secondary lymphoid organogenesis, the consequences of deleting NIK exclusively in B cells have not been determined. In this issue of the European Journal of Immunology, Hahn et al. [Eur. J. Immunol. 2016. 46: 732-741] describe mice in which the NF-κB2 pathway mediator, NIK, is deleted at different points in B-cell lineage differentiation and activation. The results show that the survival of mature peripheral B cells, as well as appropriate kinetics of germinal center reactions, rely on noncanonical NF-κB signaling. These findings confirm and extend prior observations implicating a nonredundant role for NF-κB2 downstream of BAFF signaling via BAFF-R, and prompt assessment of the growing literature regarding the relative roles of BCR and BAFF signals in B-cell homeostasis, as well as the downstream pathways responsible.
authors.affiliation: Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
authors.forename: Arpita
authors.initials: A
authors.lastname: Myles
authors.affiliation: Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
authors.forename: Michael P
authors.initials: MP
authors.lastname: Cancro
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*
chemical_list: D017346:Protein Serine-Threonine Kinases
keywords: activation ⋅ B cells ⋅ homeostasis ⋅ NF-κB-inducing kinase (NIK)