Wiley Logo Systemic lupus erythematosus (SLE) or lupus is a chronic, multisystem autoimmune disease that may trigger inflammation in the body and affect multiple organs. Investigations have pointed out that SLE patients have higher chances of being diagnosed with atherosclerosis. Chinese scientists have now found that interferon-alpha (IFN-α) is related to an increased risk of atherosclerosis in SLE patients.

It was suggested that IFN-α priming promotes lipid uptake and foam cell formation which is a vital step in plaque build-up. Activation of the IFN signaling pathway probably associates with premature atherosclerosis risk in SLE. In an attempt to highlight the seeming cause of premature atherosclerosis in SLE, investigators examined 42 patients with lupus and 42 healthy volunteers. Blood samples were gathered from all the study subjects. Also the peripheral blood monocytes were isolated and assessed. It is believed that peripheral blood mononuclear cells (PBMCs) play a crucial role in the immune system’s ability to tackle infection.

“Although traditional risk factors such as hypertension, high cholesterol, and diabetes mellitus are thought to be important in mediating an increased risk for atherosclerosis in SLE, they fail to adequately explain the higher incidence of atherosclerotic diseases in SLE patients,” said Nan Shen, M.D., Director of the Shanghai Institute of Rheumatology at Ren Ji Hospital and lead author of the study.

It was mentioned that IFN-α priming supposedly triggers the formation of macrophage-derived foam cells in SLE patients. Macrophage scavenger receptor A (SR-A) expression by IFN-α seems to be particularly linked with improved lipid uptake and an increased number of foam cells. Atherosclerosis apparently begins with the accumulation of cholesterol-laden foam cells in the arterial wall. Investigators presume that expression of SR-A is considerably raised in PBMCs of lupus patients. This elevation of SR-A may be positively correlated with IFN signaling activity. The study findings can allegedly help develop therapeutic targets for the prevention and treatment of premature cardiovascular disease in lupus patients.

The study will be published in the February issue of Arthritis and Rheumatism.