The atypical IκB protein IκBNS is important for Toll‐like receptor‐induced interleukin‐10 production in B cells
Although a major function of B cells is to mediate humoral immunity by producing antigen‐specific antibodies, a specific subset of B cells is important for immune suppression, which is mainly mediated by the secretion of the anti‐inflammatory cytokine interleukin‐10 (IL‐10). However, the mechanism by which IL‐10 is induced in B cells has not been fully elucidated. Here, we report that IκBNS, an inducible nuclear IκB protein, is important for Toll‐like receptor (TLR)‐mediated IL‐10 production in B cells. Studies using IκBNS knockout mice revealed that the number of IL‐10‐producing B cells is reduced in IκBNS −/− spleens and that the TLR‐mediated induction of cytoplasmic IL‐10‐positive cells and IL‐10 secretion in B cells are impaired in the absence of IκBNS. The impairment of IL‐10 production by a lack of IκBNS was not observed in TLR‐triggered macrophages or T‐cell‐receptor‐stimulated CD4+ CD25+ T cells. In addition, IκBNS‐deficient B cells showed reduced expression of Prdm1 and Irf4 and failed to generate IL‐10+ CD138+ plasmablasts. These results suggest that IκBNS is selectively required for IL‐10 production in B cells responding to TLR signals, so defining an additional role for IκBNS in the control of the B‐cell‐mediated immune responses.
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