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Immunity. 2009 Jun 19;30(6):802-16. doi: 10.1016/j.immuni.2009.04.013. Epub 2009 Jun 11.

Promyelocytic leukemia zinc finger protein regulates interferon-mediated innate immunity.

Author information

1
Monash Institute of Medical Research, Monash University, Melbourne, Australia.

Abstract

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 identified the promyelocytic leukemia zinc finger (PLZF) protein as a previously unrecognized component of the IFN response. IFN stimulated an association of PLZF with promyelocytic leukemia protein (PML) and histone deacetylase 1 (HDAC1) to induce a decisive subset of IFN-stimulated genes (ISGs). Consequently, PLZF-deficient mice had a specific ISG expression defect and as a result were more susceptible to viral infection. This susceptibility correlated 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.

PMID:
19523849
PMCID:
PMC2711215
DOI:
10.1016/j.immuni.2009.04.013
[Indexed for MEDLINE]
Free PMC Article

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