The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
IFN-gamma potentiates atherosclerosis in ApoE knock-out mice.
Open accessAbstract
The early colocalization of T cells and the potent immunostimulatory cytokine IFN-gamma to atherosclerotic lesions suggest that the immune system contributes to atherogenesis. Since mice with a targeted disruption of the apoE gene (apoE 0 mice) develop profound atherosclerosis, we examined the role of IFN-gamma in this process. First, the presence of CD4(+) and CD8(+) cells, which secrete lesional IFN-gamma, was documented in apoE 0 atheromata. Then, the apoE 0 mice were crossed with IFN-gamma receptor (IFNgammaR) 0 mice to generate apoE 0/IFNgammaR 0 mice. Compared to the apoE 0 mice, the compound knock-out mice exhibited a substantial reduction in atherosclerotic lesion size, a 60% reduction in lesion lipid accumulation, a decrease in lesion cellularity, but a marked increase in lesion collagen content. Evaluation of the plasma lipoproteins showed that the compound knockout mice had a marked increase in potentially atheroprotective phospholipid/apoA-IV rich particles as well. This correlated with an induction of hepatic apoA-IV transcripts. These observations suggest that IFN-gamma promotes and modifies atherosclerosis through both local effects in the arterial wall as well as a systemic effect on plasma lipoproteins. Therefore, therapeutic inhibition of IFN-gamma signaling may lead to the formation of more lipid-poor and stable atheromata.
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Metadata
- Authors
- Gupta, S., Pablo, A. M., Jiang, X. C., Wang, N., Tall, A. R., & Schindler, C.
- Venue
- Journal of Clinical Investigation
- Published
- 1997-06-01
- Volume
- 99
- Issue
- 11
- Pages
- 2752-2761
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2092834104
- Cited by
- 868
- References
- 5
- FWCI
- 11.53
- Type
- journal article
- Language
- en
- Open access
- bronze
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