Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of fatty streaks within arterial walls. In hyperlipidemic conditions, cholesterol accumulates in macrophages disrupting cholesterol trafficking and leading to an inflammatory environment. C1q plays a dual role in atherosclerosis. Activation of complement by C1q exacerbates disease by release of pro-inflammatory activation fragments C3a and C5a. However, we have shown in vitro that C1q has numerous protective roles in atherosclerosis such as improving macrophage cholesterol ingestion and efflux, and polarizing macrophages towards a resolving, anti-inflammatory phenotype. Here we investigate if C1q programs similar macrophage inflammatory responses in vivo. We hypothesize that C1q polarizes macrophages to a protective phenotype in the early stages of atherosclerosis by increasing anti-inflammatory cytokines and decreasing pro-inflammatory cytokines, leading to a reduction in disease markers such as cholesterol and triglyceride levels and atherosclerotic lesion size. To investigate, atherosclerosis model, LDLr−/−, mice that are C1q sufficient or deficient were fed a high fat Western diet for 12 weeks. Changes in plasma cyto/chemokine levels are measured by luminex multiplex assay. Cholesterol and triglyceride levels are measured by colorimetric assay. Atherosclerotic lesions are measured in H&E stained aortic sinus. Preliminary data suggests that C1q modulates disease markers as predicted. By understanding the role of C1q in atherosclerosis it may be possible to design improved treatment strategies.