Optimizing treatment strategies in psoriasis: targeting the IL-23/12 pathway = Optimizing treatment strategies in psoriasis: targeting the IL-23/12 pathway

다국어 초록 (Multilingual Abstract)

Psoriasis is an immune-mediated inflammatory disease that affects 0.5%-4% of the population according to ethnicity. Over the past decade, research into the immunopathogenesis of psoriasis, including investigations into the role of tumor necrosis factor-alpha and more recently interleukins (IL) 12/23, has led to the advent of targeted biologic therapies based on the central role of a new subset of T cells, Th17. Because of their increased specificity, biologic agents have revolutionized short- to medium-term treatment outcomes and safety profiles for moderate to severe disease over previously gold standard systemic agents. The immunopathogenesis of the disease is still a focus for researchers and novel targets for future agents are being discovered and investigated in clinical trials. In particular, specifically targeting the IL-23/Th17 pathway has given rise to IL-23p19 and IL-17 antagonists, both of which have shown significant promise in clinical trials. Interleukin (IL)-23 is a heterodimeric cytokine composed of a distinct p19 subunit and a p40 subunit, which it shares with IL-12. The aim of this presentation is to bring to light new data demonstrating clinical efficacy of targeting IL-23/12 pathway. Although current IL-12/23p40 inhibitors have shown good efficacy and safety, data regarding the functional role of IL-12 in immune defense suggest that preserving this cytokine would be beneficial. To date, evidence from mouse models and preliminary data in human beings show that specifically targeting IL-23p19 may be a safer but equally efficacious treatment option.