We have recently identified an inducible nuclear factor-B (NF-B) regulator, IB-, which is induced by microbial ligands for Toll-like receptors such as lipopolysaccharide and the proinflammatory cytokine interleukin (IL)-1␤ but not by tumor necrosis factor (TNF)-␣. In the present study, we examined mechanisms for stimulus-specific induction of IB-. The analysis of the IB-promoter revealed an essential role for an NF-B binding sequence in transcriptional activation. The activation, however, did not account for the Toll-like receptor/IL-1 receptor-specific induction of IB-, because the promoter analysis and nuclear run-on analysis indicated that its transcription was similarly induced by TNF-␣. To examine post-transcriptional regulation, we analyzed the decay of IB-mRNA, and we found that it was specifically stabilized by lipopolysaccharide or IL-1␤ but not by TNF-␣. Furthermore, we found that costimulation with TNF-␣ and another proinflammatory cytokine, IL-17, elicited the IB-induction. Stimulation with IL-17 alone did not induce IB-but stabilized its mRNA. Therefore, IB-induction requires both NF-B activation and stimulus-specific stabilization of its mRNA. Because IB-is essential for expression of a subset of NF-B target genes, the stimulus-specific induction of IB-may be of great significance in regulation of inflammatory reactions.

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OBJECTIVE. The aim of thisretrospective studywasto clarify whetherMR cholangiopan creatography (MRCP) isa suitablereplacement for ERCP in evaluation of thecholedochal cyst. MATERIALSAND METHODS. Sixteenpatients(six adultand 10pediatric)with chole dochal cysts underwent MRCP using a half-Fourier acquisition single-shot turbo spin-echo se quence. Extent of the cyst. defects within the biliary tree, and presence or absence of the anomalous junction of the pancreaticobiliary duct were evaluated. Findings were compared with those of ERCP.RESULTS. MRCP betterdefinedthe proximalbiliary tree thandid ERCP in two patients. Defectswithin the biliary tree were diagnosedcorrectlyon MRCP in eight patients;however, two defects within the distal common bile duct were missed in pediatric patients. The presence of the anomalous junction of the pancreaticobiliary duct was revealed accurately by MRCP in all adult patients but was revealed accurately in only four of the 10 pediatric patients.CONCLUSION. MRCP appearsto offer diagnosticinformationthat is equivalentto that of ERCP for assessment ofcholedochalcystsin adults.In pediatricpatients, MRCP shouldnot replace ERCP; however, MRCP can play an important role as a noninvasive examination and shouldbe considered a first-choiceimagingtechniquefor evaluationof choledochal cysts.

IκB-ζ [inhibitor of NF-κB (nuclear factor κB) ζ ] is a nuclear protein that is induced upon stimulation of TLRs (Toll-like receptors) and IL (interleukin)-1 receptor. IκB-ζ harbours Cterminal ankyrin repeats that interact with NF-κB. Our recent studies have shown that, upon stimulation, IκB-ζ is essential for the induction of a subset of inflammatory genes, represented by IL-6, whereas it inhibits the expression of TNF (tumour necrosis factor)-α. In the present study, we investigated mechanisms that determine the different functions of IκB-ζ . We found that coexpression of IκB-ζ and the NF-κB subunits synergistically activates transcription of the hBD-2 (human β-defensin 2) and NGAL (neutrophil gelatinase-associated lipocalin) genes, whereas it inhibits transcription of E-selectin. Reporter analyses indicated that, in addition to an NF-κB-binding site, a flanking C/EBP (CCAAT/enhancer-binding protein)-binding site in the promoters is essential for the IκB-ζ -mediated transcriptional activation. Using an artificial promoter consisting of the NF-κB-and C/EBP-binding sites, transcriptional activation was observed upon co-transfection with IκB-ζ and NF-κB, indicating that these sequences are minimal elements that confer the IκB-ζ -mediated transcriptional activation. Chromatin immunoprecipitation assays and knockdown experiments showed that both IκB-ζ and the NF-κB subunits were recruited to the NGAL promoter and were essential for the transcriptional activation of the hBD-2 and NGAL promoters on stimulation with IL-1β. The activation of the NGAL promoter by transfection of IκB-ζ and NF-κB was suppressed in C/EBPβ-depleted cells. Thus IκB-ζ acts as an essential transcriptional activator by forming a complex with NF-κB on promoters harbouring the NF-κB-and C/EBP-binding sites, upon stimulation of TLRs or IL-1 receptor.Key words: CCAAT/enhancer-binding protein (C/EBP), inflammation, inhibitor of nuclear factor κB ζ (IκB-ζ ), innate immunity, nuclear factor κB (NF-κB), transcription.

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