CD40LG and systemic lupus erythematosus: As an example, it has been reported that in advanced SLE vascular lesions, atherosclerotic plaques can release CD40 ligand+ (CD40L)-microvesicles which can further stimulate endothelial cell proliferation and angiogenesis, thus contributing to the transition from stable to unstable plaques and to the worsening of SLE vascular lesions (130).