Immune mediators and metabolites to stratify SLE patients at high risk of cardio vascular diseases (IMSLE)

Accelerated atherosclerosis is an established complication of systemic autoimmune diseases, particularly SLE. Young female patients with SLE are more likely to develop myocardial infarction than matched healthy controls, and CVD is nowadays one of the most common causes of death (27%) in lupus patients. While traditional CV risk factors cannot explain such increased CV morbidity associated with SLE, common disease factors shared between SLE, atherosclerosis and treatment exposure may be of outmost importance in this process. 3 findings of particular interest were found that could link SLE pathogenesis and atherosclerosis-associated immune dysregulation:
1/ specific immunometabolites (circulating nucleotide-derived metabolites) which are increased in the circualtion of SLE patients 2/ OX40L as an important costimulatory molecule implicated in follicular helper T cell (Tfh) activation in SLE 3/ Immune complexes-activated platelets sustain aberrant immune response in SLE and block immunosuppressive functions of regulatory T cells (Tregs).
Exploring these interconnected pathways in SLE patients together with traditional and other well-established disease-related factors, might lead to a better stratification of CV risk in SLE.