Immune Response in Stat2 Knockout Mice
Copyright policy )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.
- Columbia University United States
- Memorial Sloan Kettering Cancer Center United States
- King’s University United States
CD4-Positive T-Lymphocytes, Immunology, Gene Expression, CD8-Positive T-Lymphocytes, GTP Phosphohydrolases, Interferon-gamma, Mice, Rhabdoviridae Infections, Immunology and Allergy, Animals, Mice, Knockout, Interferon-alpha, STAT2 Transcription Factor, Interferon-Stimulated Gene Factor 3, Phosphoproteins, Interferon-Stimulated Gene Factor 3, gamma Subunit, DNA-Binding Proteins, Infectious Diseases, Gene Targeting, Trans-Activators, Gene Deletion, Interferon Regulatory Factor-1, Signal Transduction
CD4-Positive T-Lymphocytes, Immunology, Gene Expression, CD8-Positive T-Lymphocytes, GTP Phosphohydrolases, Interferon-gamma, Mice, Rhabdoviridae Infections, Immunology and Allergy, Animals, Mice, Knockout, Interferon-alpha, STAT2 Transcription Factor, Interferon-Stimulated Gene Factor 3, Phosphoproteins, Interferon-Stimulated Gene Factor 3, gamma Subunit, DNA-Binding Proteins, Infectious Diseases, Gene Targeting, Trans-Activators, Gene Deletion, Interferon Regulatory Factor-1, Signal Transduction
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