A deficiency of complement factors in both the classic and lectin pathway, including complement component 1q (C1q), mannose-binding lection (MBL), and complement component 3 (C3), in a low-density lipoprotein receptor-deficient (Ldlr−/−) murine model of lupus has been shown to result in larger atherosclerotic lesions. Here, LDLR is linked to systemic lupus erythematosus.