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• W2167239214 endingPage "2510" @default.
• W2167239214 startingPage "2500" @default.
• W2167239214 abstract "ABSTRACT Mycobacterium tuberculosis inhibits gamma interferon (IFN-γ)-mediated antimycobacterial action by adopting diverse mechanisms. IFN-γ binds to its receptor, IFN-γR, in order to initiate proper signaling. We have observed reduced surface expression levels of IFN-γ receptor 1 (IFN-γR1) in untreated pulmonary tuberculosis patients compared to those in healthy individuals ( P < 0.01). Following antitubercular therapy, the expression of IFN-γR1 was restored in these patients. To delineate the mechanism by which M. tuberculosis modulates IFN-γR1, in vitro experiments were designed, wherein the down modulation of IFN-γR1 surface expression was observed for CD14 + cells in peripheral blood mononuclear cells (PBMCs) cocultured with live M. tuberculosis compared to that for uninfected cells ( P < 0.01). No modulation of IFN-γR1 expression was observed for CD14 + cells in PBMCs infected with Mycobacterium smegmatis . A time-dependent decrease in IFN-γR1 mRNA expression was observed for PBMCs infected with M. tuberculosis . Similar down modulation of IFN-γR1 protein and mRNA expression in phorbol myristate acetate-differentiated THP-1 cells (pdTHP-1) by M. tuberculosis was observed ( P < 0.01). Using reporter gene analysis of 5′ deletion constructs of the IFN-γR1 gene ( IFNGR1 ) promoter, the decrease in IFN-γR1 mRNA in M. tuberculosis -infected pdTHP-1 cells was shown to be due to the decreased transcription of IFNGR1 . By immunoblotting and electrophoretic mobility shift assays, the down regulation of stimulating protein 1 (Sp1) expression and its recruitment on the phorbol ester-responsive element of the IFNGR1 promoter in M. tuberculosis -infected pdTHP-1 cells was observed. This down regulation of Sp1 in pdTHP-1 cells cocultured with M. tuberculosis may be responsible for the down regulation of IFN-γR1 expression, thereby potentially altering its receptivity to IFN-γ." @default.
• W2167239214 created "2016-06-24" @default.
• W2167239214 creator A5032337999 @default.
• W2167239214 creator A5062898470 @default.
• W2167239214 creator A5064196792 @default.
• W2167239214 creator A5089305476 @default.
• W2167239214 date "2007-05-01" @default.
• W2167239214 modified "2023-09-24" @default.
• W2167239214 title "Modulation of Gamma Interferon Receptor 1 by<i>Mycobacterium tuberculosis</i>: a Potential Immune Response Evasive Mechanism" @default.
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• W2167239214 doi "https://doi.org/10.1128/iai.01743-06" @default.
• W2167239214 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1865798" @default.
• W2167239214 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17339358" @default.
• W2167239214 hasPublicationYear "2007" @default.
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