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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Immunology 2016 ; 147 (4): 453-63 Nephropedia Template TP
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The atypical I?B protein I?BNS 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 PMID26749055show 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?BNS knockout mice revealed that the number of IL?10?producing B cells is reduced in I?BNS?/? 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?BNS. The impairment of IL?10 production by a lack of I?BNS was not observed in TLR?triggered macrophages or T?cell?receptor?stimulated CD4+CD25+ T cells. In addition, I?BNS?deficient B cells showed reduced expression of Prdm1 and Irf4 and failed to generate IL?10+CD138+ plasmablasts. These results suggest that I?BNS is selectively required for IL?10 production in B cells responding to TLR signals, so defining an additional role for I?BNS in the control of the B?cell?mediated immune responses.