| First Author | Miura M | Year | 2016 |
| Journal | Immunology | Volume | 147 |
| Issue | 4 | Pages | 453-63 |
| PubMed ID | 26749055 | Mgi Jnum | J:249715 |
| Mgi Id | MGI:5923868 | Doi | 10.1111/imm.12578 |
| Citation | Miura M, et al. (2016) The atypical IkappaB protein IkappaB(NS) is important for Toll-like receptor-induced interleukin-10 production in B cells. Immunology 147(4):453-63 |
| abstractText | 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 IkappaBNS , an inducible nuclear IkappaB protein, is important for Toll-like receptor (TLR)-mediated IL-10 production in B cells. Studies using IkappaB(NS) knockout mice revealed that the number of IL-10-producing B cells is reduced in IkappaB(NS)(-/-) 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 IkappaB(NS). The impairment of IL-10 production by a lack of IkappaB(NS) was not observed in TLR-triggered macrophages or T-cell-receptor-stimulated CD4(+) CD25(+) T cells. In addition, IkappaB(NS)-deficient B cells showed reduced expression of Prdm1 and Irf4 and failed to generate IL-10(+) CD138(+) plasmablasts. These results suggest that IkappaB(NS) is selectively required for IL-10 production in B cells responding to TLR signals, so defining an additional role for IkappaB(NS) in the control of the B-cell-mediated immune responses. |
