IL-23 and monocyte interactions redirect human Th17.1 cells to an IL-17AhighIFN-γhigh potentially pathogenic profile

Introduction

IL-23-targeted therapies have demonstrated clinical efficacy in psoriatic arthritis (PsA), primarily through the reduction of IL-17A-driven inflammation. Consequently, most studies have focused on classical, high IL-17A-producing, CCR6+CXCR3-CCR4+ Th17 cells. In contrast, the impact of IL‑23 signaling on CCR6+CXCR3+CCR4- Th17.1 cells -traditionally characterized by high IFN-γ and low IL-17A production-remains largely unexplored, despite their recognized pathogenicity in autoimmune disease. The aim of this study was to characterize the effects of IL-23 on human memory Th17.1 cells.