Table 1.

Review of SLE-Accelerated Atherosclerosis Treatments

Treatment	Effect in SLE-Accelerated Atherosclerosis	References
BAFF Inhibition	Improves SLE responder index in patients with ongoing B cell dysfunction Reduces circulating anti-dsDNA antibodies in mice Inhibits antibody and complement deposition in the kidney in mice Atheroprotective in animals with low (<5mmol/L) cholesterol and atherogenic in animals with high cholesterol	[52,54**]
Hydroxychloroquine	Reduces interferon-α production Lessens aortic stiffness in SLE patients Corrects lipoprotein profile (increases HDL and lowers cholesterol, LDL, VLDL, triglycerides, and cylomicrons) in SLE patients Improves glycemic control in non-diabetic women with SLE Reduces the risk of all thrombovascular events in SLE patients SLE patients with carotid plaque are less likely to be using HCQ than those with no plaque (63% vs. 82.3%) Long term HCQ treatment in ApoE−/− mice with pristane-induced SLE reduces atherosclerotic lesion size, anti-dsDNA antibodies, total leukocyte numbers, macrophages, and DCs, and increases lymohocytes HDL from SLE patients is more functional following 12 weeks of treatment with HCQ.	[58–67*,70*]
Low-dose IL-2	IL-2 treatment reduces renal inflammation and activation of kidney-infiltrating CD4+ T cells in a mouse model of lupus nephritis Targeted IL-2 treatment in ApoE−/− mice reduces the size of pre-established atherosclerotic lesions Currently under study in clinical trials to determine its effectiveness in SLE and atherosclerosis	[96*,97–99]
Mycophenolate	Treatment with MMF for 12 weeks improves HDL function in SLE patients Treatment with MMF for 12 weeks improves CVD biomarkers like sTWEAK in SLE patients Reduces atherosclerosis in Ldlr−/− B6.Sle1.2.3 bone marrow chimeras and limits recruitment of CD4+ T cells to atherosclerotic lesions	[70*,71]

VLDL = very low-density lipoprotein