Atherosclerosis is a chronic lipid-driven inflammatory disease of the arterial wall. Interferon gamma (IFN?) is an important immunomodulatory cytokine and a known pro-atherosclerotic mediator. However, cell-specific targeting of IFN? or its signaling in atherosclerosis development has not been studied yet. As macrophages are important IFN? targets, we here addressed the involvement of myeloid IFN? signaling in murine atherosclerosis.Bone marrow was isolated from interferon gamma receptor 2 chain (IFN?R2) wildtype and myeloid IFN?R2 deficient mice and injected into lethally irradiated LDLR(-/-) mice. After recovery mice were put on a high fat diet for 10 weeks after which atherosclerotic lesion analysis was performed. In addition, the accompanying liver inflammation was assessed.Even though absence of myeloid IFN? signaling attenuated the myeloid IFN? response, no significant differences in atherosclerotic lesion size or phenotype were found. Also, when examining the liver inflammatory state no effects of IFN?R2 deficiency could be observed.Overall, our data argue against a role for myeloid IFN?R2 in atherosclerosis development. Since myeloid IFN? signaling seems to be nonessential throughout atherogenesis, it is important to understand the mechanisms by which IFN? acts in atherogenesis. In the future new studies should be performed considering other cell-specific targets.
- Interferon gamma receptor
- Mouse model