IL23driven

IL23driven refers to inflammatory processes that are predominantly powered by the cytokine interleukin-23 (IL-23). IL-23 is produced by activated antigen-presenting cells and functions as a heterodimer composed of a p19 subunit and a p40 subunit that it shares with IL-12. The IL-23 receptor is expressed on various immune cells, including T helper 17 (Th17) cells and certain innate lymphoid cells, enabling IL-23 to influence both adaptive and innate immune responses.

The central mechanism of IL-23–driven inflammation involves the expansion, maintenance, and stabilization of Th17 cells, which secrete inflammatory mediators such as IL-17A, IL-17F, and IL-22, among others. IL-23 can also impact the activity of other cell types, including macrophages and neutrophils, contributing to a chronic inflammatory milieu. The axis often interacts with other cytokines, including TNF-α, amplifying tissue inflammation in susceptible contexts.

IL-23–driven pathology is implicated in several autoimmune and inflammatory diseases. Notable examples include psoriasis, psoriatic arthritis, inflammatory bowel diseases (Crohn’s disease and ulcerative colitis), and ankylosing spondylitis. The IL-23/Th17 axis is a focus of therapeutic development, with several drugs targeting this pathway. Anti-IL-23 therapies that block the p19 subunit (such as guselkumab, risankizumab, and tildrakizumab) have demonstrated efficacy in skin and gut diseases, while agents blocking both IL-12 and IL-23 (such as ustekinumab) are used in a range of inflammatory conditions. Ongoing research continues to delineate the specific roles of IL-23 in different tissues and disease contexts.