| First Author | Bellini R | Year | 2023 |
| Journal | Atheroscler Plus | Volume | 51 |
| Pages | 8-12 | PubMed ID | 36969702 |
| Mgi Jnum | J:345136 | Mgi Id | MGI:7581083 |
| Doi | 10.1016/j.athplu.2022.12.001 | Citation | Bellini R, et al. (2023) Dendritic cell marker Clec4a4 deficiency limits atherosclerosis progression. Atheroscler Plus 51:8-12 |
| abstractText | BACKGROUND AND AIMS: Atherogenesis results from altered lipid metabolism and impaired immune response. Emerging evidence has suggested that dendritic cells (DCs) participate to atherosclerosis-related immune response, but their impact is scarcely characterized. Clec4a4 or DCIR2 (Dendritic cell immunoreceptor 2) is a C-type lectin receptor, mainly expressed by CD8alpha(-) DCs, able to modulate T cell immunity. However, whether this DC subset could play a role in the atherogenesis is still poorly understood. Thus, the aim of this study is to investigate whether the absence of Clec4a4 could affect atherosclerosis-related immune response and atherosclerosis itself. METHODS: Dcir2 (-/-) Ldlr (-/-) and Ldlr (-/-) mice were fed a standard diet or cholesterol-enriched diet for 12 weeks. Subsequently, the profile of circulating and lymph nodes-resident immune cells was investigated together with the analysis of plasma lipid levels and atherosclerotic plaque extension in the aorta. RESULTS: Here, we show that Clec4a4 expression is downregulated under hypercholesterolemia and its deficiency in Ldlr (-/-) mice results in the reduction of atherosclerotic plaque formation, together with altered lipid metabolism and impaired myeloid immune cell distribution. CONCLUSIONS: Our findings suggest a pro-atherosclerotic role of Clec4a4 in experimental atherosclerosis. |
