IL-23

IL-23 is a heterodimeric cytokine of the IL-12 family composed of the p19 and p40 subunits and functions as a central regulator of inflammatory immune responses through the IL-23/IL-17 axis.^[1] Mechanistically, IL-23 is produced primarily by antigen-presenting myeloid cells and promotes the proliferation, survival, and stabilization of pathogenic T helper 17 (Th17) cells, thereby sustaining production of pro-inflammatory effector cytokines and amplifying downstream inflammatory signaling.^[2][3] Through these activities, IL-23 contributes to tissue inflammation, barrier immune responses, and the maintenance of chronic immune-mediated inflammatory processes.^[2][4] Disease-associated studies have identified IL-23 as a critical pathogenic cytokine in psoriasis, psoriatic arthritis, inflammatory bowel disease, and other inflammatory disorders in which dysregulation of the IL-23/IL-17 pathway is observed.^[2][3][5] Compared with the related cytokine IL-12, which shares the p40 subunit but contains a p35 subunit, IL-23 exhibits distinct biological functions and is more closely associated with Th17-cell maintenance, whereas IL-12 is linked to Th1-cell responses.^[1][2] Experimental studies using cytokine-deficient models demonstrated that IL-23-driven inflammatory mechanisms are pathogenetically distinct from those mediated by IL-12.^[2] For experimental and translational research applications, monoclonal antibodies targeting either the shared p40 subunit or the IL-23-specific p19 subunit have enabled selective interrogation and therapeutic inhibition of IL-23 signaling in inflammatory disease models and clinical settings.^[5]