| http://purl.uniprot.org/citations/17030574 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17030574 | http://www.w3.org/2000/01/rdf-schema#comment | "Gamma interferon (IFN-gamma)-induced indoleamine dioxygenase (IDO), which inhibits chlamydial replication by reducing the availability of tryptophan, is up-regulated by interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). The mechanisms by which this occurs include an increase in the synthesis of interferon regulatory factor-1 as well as a nuclear factor-kappaB (NF-kappaB)-dependent increase in the expression of IFN-gamma receptors (IFN-gammaR). Although Chlamydia is susceptible to IDO, it up-regulates IFN-gammaR expression to a greater degree than either IL-1beta or TNF-alpha, perhaps through interaction with Toll-like receptors (TLR). The purpose of this study was to determine the mechanism by which Chlamydia psittaci up-regulates IFN-gammaR expression and evaluate this effect on IDO induction. Infection of HEK 293 cells with C. psittaci increased IFN-gammaR expression only in cells expressing either TLR2 or TLR4 and the adaptor protein MD-2. In addition, up-regulation of IFN-gammaR expression in Chlamydia-infected HeLa cells could be blocked either by neutralizing TLRs with anti-TLR2 and/or anti-TLR4 or by inhibiting NF-kappaB transactivation with a proteasome inhibitor. Although the newly expressed IFN-gammaR in Chlamydia-infected cells were capable of binding IFN-gamma, they did not enhance IFN-gamma-induced IDO activity in a manner similar to those observed for IL-1beta and TNF-alpha. Instead, IDO activation in Chlamydia-infected cells was no different than that induced in uninfected cells, despite the increase in IFN-gammaR expression. Furthermore, the amount of IFN-gamma-induced signal transducer and activator of transcription 1 (STAT-1) activation in infected cells paralleled that observed in uninfected cells, suggesting that STAT-1 activation by these newly expressed receptors was impaired."xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.org/dc/terms/identifier | "doi:10.1128/iai.00505-06"xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/author | "Jung J.Y."xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/author | "Carlin J.M."xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/author | "Shirey K.A."xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/name | "Infect Immun"xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/pages | "6877-6884"xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/title | "Up-regulation of gamma interferon receptor expression due to Chlamydia-toll-like receptor interaction does not enhance signal transducer and activator of transcription 1 signaling."xsd:string |
| http://purl.uniprot.org/citations/17030574 | http://purl.uniprot.org/core/volume | "74"xsd:string |
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