Pathogenic immunity in systemic lupus erythematous and atherosclerosis: common mechanisms

Systemic lupus erythematous (SLE) is an autoimmune syndrome primarily affecting young women characterized by inflammation in several organs including kidneys, skin, joints, blood and the nervous system. Abnormal immune cellular and humoral responses play key roles in the development of the disease process. Impaired clearance of apoptotic material is a key factor contributing to activation of self-reactive immune cells. The incidence of atherosclerotic cardiovascular disease (CVD) is increased with up to 50 times in SLE patients compared to age and gender-matched controls and this can only partly be explained by traditional risk factors for CVD. Currently, there is no effective treatment to prevent CVD complications in SLE. Traditional preventive CVD therapies have not proven to significantly lower the incidence of CVD in SLE; therefore, there is a need for novel treatment strategies and increased understanding of the mechanisms involved in CVD complications in SLE. The pathogenic immune responses in SLE and development of atherosclerotic plaques share some similar characteristics, such as impaired efferocytosis and skewed T cell activation, suggesting the possibility to identify novel targets for intervention. As novel immune-based therapies for CVD are being developed and brought into clinical testing, it is possible that some of these may also show efficacy in CVD prevention and immunomodulation in SLE. However, further understanding of the mechanisms leading to increased CVD in SLE is critical for development of such therapies.