Abstract：
BACKGROUND AND AIMS:Atherosclerosis is a chronic lipid-driven inflammatory disease of the arterial wall. Interferon gamma (IFNγ) is an important immunomodulatory cytokine and a known pro-atherosclerotic mediator. However, cell-specific targeting of IFNγ or its signaling in atherosclerosis development has not been studied yet. As macrophages are important IFNγ targets, we here addressed the involvement of myeloid IFNγ signaling in murine atherosclerosis. METHODS:Bone marrow was isolated from interferon gamma receptor 2 chain (IFNγR2) wildtype and myeloid IFNγR2 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. RESULTS:Even though absence of myeloid IFNγ signaling attenuated the myeloid IFNγ response, no significant differences in atherosclerotic lesion size or phenotype were found. Also, when examining the liver inflammatory state no effects of IFNγR2 deficiency could be observed. CONCLUSION:Overall, our data argue against a role for myeloid IFNγR2 in atherosclerosis development. Since myeloid IFNγ signaling seems to be nonessential throughout atherogenesis, it is important to understand the mechanisms by which IFNγ acts in atherogenesis. In the future new studies should be performed considering other cell-specific targets.
journal_name
Atherosclerosisjournal_title
Atherosclerosisauthors
Boshuizen MC,Neele AE,Gijbels MJ,van der Velden S,Hoeksema MA,Forman RA,Muller W,Van den Bossche J,de Winther MPdoi
10.1016/j.atherosclerosis.2016.01.026subject
Has Abstractpub_date
2016-03-01 00:00:00pages
325-33eissn
0021-9150issn
1879-1484pii
S0021-9150(16)30026-0journal_volume
246pub_type
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