Vulnerability of XXXX plaques is as-sociated with type I interferon in a @entity19 model of @entity1252 and @entity731 .

@entity1 @entity23310 @entity6970 @entity1885 @entity19 @entity1252 @entity1977 @entity16307 @entity731 @entity65
This study aimed to investigate the relationship between type I interferon (IFN-I) and plaque stability in @entity16307 -treated @entity6970 -knockout ( @entity6970 (-/-)) mice. Antinuclear antibody (ANA) and extractable nuclear antigen antibody (ENA) levels were measured by immunofluorescence and enzyme-linked immunospot assay. @entity731 were detected by Sirius red/fast green staining. Cell apoptosis was detected by terminal deoxynucleotidyltransferase-mediated @entity1977 - @entity1885 nick-end labeling. Gene expression was determined by real-time PCR analyses. We found that @entity16307 -treated @entity6970 (-/-) @entity19 developed @entity1252 characterized by an increased production of serum ANA and ENA. @entity16307 treatment decreased the collagen content and increased the number of apoptotic cells in plaques. Moreover, IFN-induced @entity23310 , IFIT1-1, and IFIT1-2 gene expression was increased in peripheral blood cells and aortic plaques. An IFN-a-stimulated macrophage supernatant inhibited collagen type I, alpha 1 gene expression in vascular smooth muscle cells. We concluded that the vulnerability of plaques was associated with the activation of IFN-I in @entity16307 -treated @entity6970 (-/-) @entity19 . Thus, we speculated that the higher prevalence of @entity65 in @entity1 with @entity1252 could be due to plaque instability.
