کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3376052 | 1219706 | 2007 | 6 صفحه PDF | دانلود رایگان |

SummaryMonocytes become susceptible to respiratory syncytial virus (RSV) infection when pretreated with phorbol 12-myristate 13-acetate (PMA). The molecular mechanism underlying this observation is poorly understood, but may be related to inhibition of type I interferon (IFN) signaling by RSV in epithelial cells. Herein, we have investigated the putative role of suppressor of cytokine signaling (SOCS) in the IFN-inducible antiviral response in U937 cells. Upon RSV infection of macrophage-like U937 cells, the expression of SOCS1, SOCS3, and CIS mRNA was rapidly upregulated, and phosphorylation of the IFN-α-inducible signal transducer and activator of transcription (STAT1 and STAT2) was suppressed. These results suggest that RSV can inhibit the phosphorylation of IFN-α-inducible STAT1 and STAT2 by inducing the expression of SOCS proteins in PMA-treated U937 cells.
Journal: Journal of Infection - Volume 54, Issue 4, April 2007, Pages 393–398