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The atypical I?B protein I?B(NS) is important for Toll-like receptor-induced
interleukin-10 production in B cells
#MMPMID26749055
Miura M
; Hasegawa N
; Noguchi M
; Sugimoto K
; Touma M
Immunology
2016[Apr]; 147
(4
): 453-63
PMID26749055
show ga
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 I?BNS , an
inducible nuclear I?B protein, is important for Toll-like receptor (TLR)-mediated
IL-10 production in B cells. Studies using I?B(NS) knockout mice revealed that
the number of IL-10-producing B cells is reduced in I?B(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 I?B(NS). The impairment of
IL-10 production by a lack of I?B(NS) was not observed in TLR-triggered
macrophages or T-cell-receptor-stimulated CD4(+) CD25(+) T cells. In addition,
I?B(NS)-deficient B cells showed reduced expression of Prdm1 and Irf4 and failed
to generate IL-10(+) CD138(+) plasmablasts. These results suggest that I?B(NS) is
selectively required for IL-10 production in B cells responding to TLR signals,
so defining an additional role for I?B(NS) in the control of the B-cell-mediated
immune responses.
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