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- W4313356412 abstract "Abstract Fcgamma receptors (FcγRs) are classified as activating (FcγRI, III, and IV) and inhibitory (FcγRII) receptors. Others and we have demonstrated that combined deficiency of all the three activating FcγRs (I, III and IV) in apolipoprotein E (apoE)-Fcγ chain double knockout (dKO) mice decreased atherosclerosis. In this report, we investigated the independent role of FcγRI and FcγRIV in the progression of atherosclerosis. We tested the hypothesis that FcγRI and FcγRIV exacerbate atherosclerosis using apoE-FcγRI dKO and apoE-FcγRIV dKO mice. Our results show that arterial lesions were not different between apoE-FcγRI dKO and apoE knockout (apoE KO) mice. Interestingly, arterial lesions were significantly decreased in a regular chow or a high-fat diet fed apoE-FcγRIV dKO male and female mice, relative to apoE KO mice. Bone marrow chimeras were used to address the relative contribution of FcγRIV expressed on hematopoietic cells including macrophages and dendritic cell. ApoE KO mice transplanted with apoE-FcγRIV dKO marrow showed significantly reduced arterial lesions relative to recipient mice transplanted with apoE KO marrow. Next, we investigated whether pro-inflammatory response contributed to the pro-atherogenic effect of FcγRIV. Activated CD4+ T cells of apoE-FcγRIV dKO mice showed increased secretion of IL-10, whereas IFN-γ and IL-17 by T cells were decreased. Interestingly, dendritic cells at the lesion-prone vascular site from apoE-FcγRIV dKO mice induced increased IL-10 secretion by LDL-specific T cells. Collectively, our findings suggest that the pro-inflammatory responses initiated by FcγRIV, one of the activating FcγRs, contribute to the progression of atherosclerosis. Supported by NIH grant HL086674." @default.
- W4313356412 created "2023-01-06" @default.
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- W4313356412 date "2016-05-01" @default.
- W4313356412 modified "2023-09-28" @default.
- W4313356412 title "Mouse Fcgamma Receptor IV dependent inflammatory cytokine and chemokine response contributes to progression of atherosclerosis in apoE hyperlipidemic mice" @default.
- W4313356412 doi "https://doi.org/10.4049/jimmunol.196.supp.124.6" @default.
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