| Literature DB >> 15568025 |
Hideyuki Yoshida1, Yasutaka Okabe, Kohki Kawane, Hidehiro Fukuyama, Shigekazu Nagata.
Abstract
The livers of DNase II-deficient mouse embryos contain many macrophages carrying undigested DNA, and the embryos die in utero. Here we report that erythroid precursor cells underwent apoptosis in the livers of DNase II-deficient embryos and that in the liver, interferon-beta mRNA was expressed by the resident macrophages. When the DNase II-deficient mice were crossed with mice deficient in type I interferon receptor, the resultant 'double-mutant' mice were born healthy. The double-mutant embryos expressed interferon-beta mRNA, but the expression of a subset of the interferon-responsive genes dysregulated in DNase II-deficient embryos was restored to normal. These results indicate that the inability to degrade DNA derived from erythroid precursors results in interferon-beta production that induces expression of a specific set of interferon-responsive genes associated with embryonic lethality in DNase II-deficient mice.Entities:
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Year: 2004 PMID： 15568025 DOI： 10.1038/ni1146
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606