C-reactive protein (CRP) is an acute-phase protein whose concentration rises sharply during the inflammatory response (1000-fold). CRP belongs to the pentraxin family of proteins, of which a key property is the ability to opsonize apoptotic cells, which can then undergo phagocytosis without triggering an inflammatory response, in marked contrast to the phagocytosis of necrotic cells. The low CRP concentrations in patients with systemic lupus erythematosus (SLE) may contribute to defective clearance of apoptotic particles, thereby promoting the development of autoimmunity to apoptotic vesicle components. In normal populations, serum CRP concentrations remain below 5–10mg/L. Within this normal range, five quintiles of CRP concentrations can be distinguished using an ultrasensitive CRP assay. Individuals who are consistently within the highest quintile are at higher risk for cardiovascular death and recurrent myocardial infarction than are individuals in the lowest quintile. Thus, the ultrasensitive CRP concentration (US-CRP) is a cardiovascular risk factor, together with the classic risk factors identified by the Framingham studies. CRP plays a role in atheroma plaque development via its ability to attract macrophages, which convert to foam cells. Any chronic inflammatory disease associated with increased CRP production can accelerate the development of atheroma. Paradoxically, the inflammatory process in patients with SLE is associated with a fairly small elevation of serum CRP concentrations. Nevertheless, this elevation is sufficient to increase the cardiovascular risk. Anti-CRP autoantibodies, which are found in 35 to 40% of SLE patients, increase the cardiovascular risk by interacting with the monomeric (degraded) form of CRP. CRP/anti-CRP immune complexes developed in the arterial wall may promote growth of the atheroma plaque.