Npgrj_ni_1287 1..7

نویسندگان

  • Jennifer E Fenner
  • Robyn Starr
  • Ann L Cornish
  • Jian-Guo Zhang
  • Donald Metcalf
  • Robert D Schreiber
  • Kathleen Sheehan
  • Douglas J Hilton
  • Warren S Alexander
  • Paul J Hertzog
چکیده

Suppressor of cytokine signaling 1 (SOCS1) is a critical regulator of cytokine signaling and immune responses. SOCS1-deficient mice develop severe inflammatory disease, but are very resistant to viral infections. Using neutralizing antibody to type I interferon (IFN-a and IFN-b) and mice deficient in interferon-c or type I interferon receptor components (IFNAR1 or IFNAR2), we demonstrate here that SOCS1 deficiency amplified type I interferon antiviral and proinflammatory actions independently of interferon-c. The mechanism of the suppression of type I interferon responses by SOCS1 was distinct from that of other cytokines. SOCS1 associated with and regulated IFNAR1but not IFNAR2-specific signals, abrogating tyrosine phosphorylation of transcription factor STAT1 and reducing the duration of antiviral gene expression. Thus, SOCS1 is an important in vivo inhibitor of type I interferon signaling and contributes to balancing its beneficial antiviral versus detrimental proinflammatory effects on innate immunity.

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تاریخ انتشار 2005