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- W2034643046 abstract "Interleukin‐10 (IL‐10) has been used in the treatment of viral hepatitis in interferon‐α (IFN‐α) non‐responders while patients who have high levels of IL‐10 are poorly responsive to IFN‐α. The mechanism underlying such controversial functions of IL‐10 remains unknown. Here we demonstrated that injection of IL‐10 into mice attenuated IFN‐α‐induced signal transducer and activator transcription factor (STAT)1 tyrosine phosphorylation in the liver. Reverse transcriptase‐polymerase chain reaction assay demonstrated that mouse liver expressed high levels of IL‐10 receptor 2 (IL‐10R2) but low levels of IL‐10R1. Injection of IL‐10 into mice activated STAT3 but not STAT1 tyrosine phosphorylation and induced suppressor of cytokine signal 2 (SOCS2), SOCS3, and cytokine‐inducible SH2 protein (CIS) mRNA expression in the liver. Furthermore, overexpression of SOCS2 or SOCS3 inhibited IFN‐α‐induced reporter activity in hepatic cells. These findings suggest that IL‐10 inhibits IFN‐α‐activated STAT1 in the liver, at least in part, by inducing SOCS2, SOCS3, and CIS expression, which may be responsible for the resistance of IFN‐α therapy in patients who have high levels of IL‐10 and recommends that IL‐10 treatment for viral hepatitis should be cautious." @default.
- W2034643046 created "2016-06-24" @default.
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- W2034643046 date "2000-08-30" @default.
- W2034643046 modified "2023-10-15" @default.
- W2034643046 title "IL-10 attenuates IFN-α-activated STAT1 in the liver: involvement of SOCS2 and SOCS3" @default.
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- W2034643046 doi "https://doi.org/10.1016/s0014-5793(00)01905-0" @default.
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