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首页> 外文期刊>Infection and immunity >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
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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

机译：由于衣原体-Toll样受体相互作用而导致的γ干扰素受体表达的上调不能增强信号转导和转录1信号的激活因子。

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Gamma interferon (IFN-γ)-induced indoleamine dioxygenase (IDO), which inhibits chlamydial replication by reducing the availability of tryptophan, is up-regulated by interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α). The mechanisms by which this occurs include an increase in the synthesis of interferon regulatory factor-1 as well as a nuclear factor-κB (NF-κB)-dependent increase in the expression of IFN-γ receptors (IFN-γR). Although Chlamydia is susceptible to IDO, it up-regulates IFN-γR expression to a greater degree than either IL-1β or TNF-α, 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-γR expression and evaluate this effect on IDO induction. Infection of HEK 293 cells with C. psittaci increased IFN-γR expression only in cells expressing either TLR2 or TLR4 and the adaptor protein MD-2. In addition, up-regulation of IFN-γR expression in Chlamydia-infected HeLa cells could be blocked either by neutralizing TLRs with anti-TLR2 and/or anti-TLR4 or by inhibiting NF-κB transactivation with a proteasome inhibitor. Although the newly expressed IFN-γR in Chlamydia-infected cells were capable of binding IFN-γ, they did not enhance IFN-γ-induced IDO activity in a manner similar to those observed for IL-1β and TNF-α. Instead, IDO activation in Chlamydia-infected cells was no different than that induced in uninfected cells, despite the increase in IFN-γR expression. Furthermore, the amount of IFN-γ-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.
机译：γ干扰素（IFN-γ）诱导的吲哚胺双加氧酶（IDO）通过减少色氨酸的可用性来抑制衣原体复制，并被白介素-1β（IL-1β）和肿瘤坏死因子α（TNF-α）上调。发生这种情况的机制包括干扰素调节因子1合成的增加以及IFN-γ受体（IFN-γR）的表达依赖核因子-κB（NF-κB）的增加。尽管衣原体对IDO敏感，但它可能通过与Toll样受体（TLR）相互作用而比IL-1β或TNF-α上调IFN-γR的表达。这项研究的目的是确定衣原体衣原体上调IFN-γR表达的机制，并评估这种对IDO诱导的作用。 HEK 293细胞感染 C。 psittaci 仅在表达TLR2或TLR4和衔接蛋白MD-2的细胞中增加IFN-γR的表达。此外，可以通过用抗TLR2和/或抗TLR4中和TLR或通过用NFκB抑制NF-κB反式激活来阻止衣原体感染的HeLa细胞中IFN-γR表达的上调。蛋白酶体抑制剂。尽管在感染了衣原体的细胞中新表达的IFN-γR能够结合IFN-γ，但它们并未以类似于对IL-1β和IL-1β观察到的方式增强IFN-γ诱导的IDO活性。 TNF-α。取而代之的是，尽管IFN-γR表达增加，但感染衣原体的细胞中的IDO激活与未感染细胞中的IDO激活没有区别。此外，受感染细胞中IFN-γ诱导的信号转导子和转录激活因子1（STAT-1）的激活与未感染细胞中观察到的平行，表明这些新表达的受体对STAT-1的激活受到了损害。

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