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Immune response in Stat2 knockout mice.

Type I IFNs induce gene expression through Stat1 and Stat2, which can in turn associate either to form Stat1 homodimers or the transcription factor ISGF-3. Stat1 homodimers also transduce signals for IFN-gamma. To explore the unique properties of Stat2 and ISGF-3 in type I IFN signaling, its gene was targeted for deletion. Stat2 null mice exhibit a number of defects in immune response. This includes an increased susceptibility to viral infection and the loss of a type I IFN autocrine/ paracrine loop, which in turn regulates several aspects of immune response. Intriguingly, Stat2-deficient fibroblasts exhibit a more significant defect in their response to type I IFNs than macrophages, highlighting tissue-specific differences in the response to this family of ligands.

Pubmed ID: 11163195


  • Park C
  • Li S
  • Cha E
  • Schindler C



Publication Data

December 19, 2000

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM54686
  • Agency: NHLBI NIH HHS, Id: HL56984

Mesh Terms

  • Animals
  • CD4-Positive T-Lymphocytes
  • CD8-Positive T-Lymphocytes
  • DNA-Binding Proteins
  • GTP Phosphohydrolases
  • Gene Deletion
  • Gene Expression
  • Gene Targeting
  • Interferon Regulatory Factor-1
  • Interferon-Stimulated Gene Factor 3
  • Interferon-Stimulated Gene Factor 3, gamma Subunit
  • Interferon-alpha
  • Interferon-gamma
  • Mice
  • Mice, Knockout
  • Phosphoproteins
  • Rhabdoviridae Infections
  • STAT2 Transcription Factor
  • Signal Transduction
  • Trans-Activators
  • Transcription Factors
  • Vesicular stomatitis Indiana virus