Author: Xu, Dakang; Holko, Michelle; Sadler, Anthony J.; Scott, Bernadette; Higashiyama, Shigeki; Berkofsky-Fessler, Windy; McConnell, Melanie J.; Pandolfi, Pier Paolo; Licht, Jonathan D.; Williams, Bryan R.G.
Title: Promyelocytic Leukemia Zinc Finger Protein Regulates Interferon-Mediated Innate Immunity Cord-id: 7bb103k7 Document date: 2009_6_1
ID: 7bb103k7
Snippet: Interferons (IFNs) direct innate and acquired immune responses and, accordingly, are used therapeutically to treat a number of diseases, yet the diverse effects they elicit are not fully understood. Here we identify the promyelocytic leukemia zinc finger (PLZF) protein as a previously unrecognized component of the IFN response. IFN stimulates an association between PLZF, the promyelocytic leukemia protein and histone deacetylase 1, to induce a decisive subset of IFN-stimulated genes (ISGs). Cons
Document: Interferons (IFNs) direct innate and acquired immune responses and, accordingly, are used therapeutically to treat a number of diseases, yet the diverse effects they elicit are not fully understood. Here we identify the promyelocytic leukemia zinc finger (PLZF) protein as a previously unrecognized component of the IFN response. IFN stimulates an association between PLZF, the promyelocytic leukemia protein and histone deacetylase 1, to induce a decisive subset of IFN-stimulated genes (ISGs). Consequently, PLZF-deficient mice have a specific ISG defect and as a result are more susceptible to viral infection. This susceptibility correlates with a marked decrease in the expression of the key antiviral mediators and an impaired IFN-mediated induction of natural killer cell function. These results provide new insights into the regulatory mechanisms of IFN signaling and the induction of innate antiviral immunity.
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