Cytokine pathways in psoriasis and psoriatic arthritis

Abstract

Psoriatic disease is a systemic autoimmune disease mostly associated with skin and joint involvement (psoriatic arthritis). Strong evidences from clinical studies and experimental models suggest that both innate and adaptive immune responses are involved in its pathogenesis. Psoriatic disease used to be regarded as a Th1-driven disease, now there are substantial evidences to suggest regulatory role of Th17 cells as well in the pathogenesis of psoriasis and psoriatic arthritis. Cytokines play a critical role; besides IFN-γ and TNFα, IL-23/Th17 pathway plays a dominant role in the infl ammatory and proliferative cascades of both the skin and joint tissues. Recently in a series of elegant experiments using mouse models and human tissues it has been demonstrated that IL-23 induced Th17 cytokines (IL-17 and IL-22) can contribute to all four pathologic events in a psoriatic disease: development of psoriatic plaque, pannus formation in the joint, joint erosion and new bone formation.