T helper 17 cells and group 3 innate lymphoid cells define a spectrum of psoriasis endotypes.

Psoriasis is a prototypical chronic inflammatory skin disease that illustrates fundamental interactions between innate and adaptive immune pathways. Central to its pathophysiology is the interleukin-23/interleukin-17 (IL-23/IL-17) axis, which is driven by both adaptive T helper 17 (Th17) cells and group 3 innate lymphoid cells (ILC3s). These cell populations share the ability to produce IL-17A, IL-17F, and IL-22, cytokines that activate keratinocytes, promote epidermal hyperproliferation, and sustain the inflammatory microenvironment characteristic of psoriatic lesions. While Th17 cells arise from antigen-driven adaptive immune responses and contribute to the persistence of chronic inflammation, ILC3s respond rapidly to cytokine signals such as IL-23 and provide an early, antigen-independent source of IL-17 and IL-22. The functional overlap and extensive crosstalk between these two cell types create a robust and self-amplifying inflammatory circuit. Increasing evidence suggests that psoriasis comprises immunological endotypes in which either Th17 cells or ILC3s may predominate, potentially contributing to clinical heterogeneity and differential responses to targeted therapies. Because psoriasis exemplifies the cooperation between innate and adaptive IL-17-producing lymphocytes, it provides a valuable model for understanding immune regulation in chronic inflammatory and autoimmune diseases. Elucidating the balance, redundancy, and plasticity between Th17 cells and ILC3s may therefore help refine disease stratification and guide future precision-based therapeutic strategies.