Atherosclerosis has been widely recognized as a slow progressing inflammatory disease of the aorta and other large caliber arterial
vessels. Accumulating evidence suggest that interleukin (IL)-35 can represent an attractive target for future anti-atherosclerotic
therapy due to several atheroprotective properties. First, immunosuppressive and anti-inflammatory activity of this cytokine could be
beneficial against vascular inflammation. Second, IL-35 can suppress a variety of T cells including proinflammatory Th1 and Th17 cells
and probably dendritic cells. Third, IL-35 supports proliferation of regulatory T cells (Tregs), increases their inhibitory function, and induces
a new set of Tregs called inducible IL-35-producing Tregs (iTr35 cells). Fourth, this cytokine promotes production of antiinflammatory
cytokines such as IL-10 and down-regulates expression of proinflammatory cytokines such as IL-17. Finally, IL-35 is inducible.
The fact that IL-35 could be induced by simple compounds such as chemical chaperons may provide advances in developing
new efficient strategies for treatment of atherosclerosis. However, it is necessary to test IL-35-inducing factors in order to understand
mechanisms of induction and then select the most optimal one. Probably, constructing of humanized antibodies that mimic IL-35 function
may provide benefits for advanced atheroprotective therapy.