Interleukin-23: A New Atherosclerosis Target

Accumulating evidence has shown that atherosclerosis is an inflammatory disease. The pathogenesis of atherosclerosis has been confirmed to involve an imbalance in anti-inflammatory/proinflammatory processes. Interleukin-23 (IL-23) is a heterodimeric cytokine composed of the IL-23p19 and IL-12p40 subunits of the IL-12 family. Experiments show that IL-23 induces CD4(+) T cells to differentiate into T helper type 17 cells, promotes the expression of interferon-gamma, and inhibits the production of Foxp3. Therefore, IL-23 induces and exacerbates effector T lymphocyte/regulatory T cell imbalance. IL-23 receptor (IL-23R) is expressed not only in T cells but also in dendritic cells (DCs) and macrophages. IL-23R can enhance its antigen-presenting ability through the autocrine pathway, enabling it to infiltrate lesion sites, promote its secretion of a large number of inflammatory factors, and upregulate proinflammatory DCs and macrophages. IL-23 binds IL-23R on the surface of target cells and transmits signals through Janus kinase 2/signal transducer and activator of transcription channels, participating in the occurrence of chronic inflammatory diseases and autoimmune diseases. Therefore, the use of IL-23 or IL-23R is a potential therapeutic approach for treating inflammatory diseases, including atherosclerosis. In this article, we hypothesize that IL-23 may be a novel target for the treatment of atherosclerosis, and further study is needed to determine the precise role of IL-23 in atherosclerosis and the associated signaling pathways.