Role of IL-17 in the pathogenesis of psoriatic arthritis and axial spondyloarthritis.

Abstract

Th17 cells are a discrete subset of T cell subpopulation, which produce IL-17 and certain other pro-inflammatory cytokines. A regulatory role of Th17 cells have been proposed in several autoimmune diseases including psoriasis, psoriatic arthritis (PsA), ankylosing spondylitis (AS), rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and multiple sclerosis. Psoriatic disease is an autoimmune disease which mainly involves skin and joints. Until recently, psoriasis and PsA were thought to be Th1 mediated disease, but after the discovery of IL-17 and IL-17 knockout animal studies as well as human experimental data indicate a crucial role of the Th17 cells in the pathogenesis of psoriasis and PsA. Our research group have not only found abundance of CD4(+)IL-17(+) T cells, mainly the memory phenotype (CD4RO(+)CD45RA(-)CD11a(+)) in the synovial fluid, but also have shown the existence of a functional IL-17 receptor in synovial fibroblast of psoriatic arthritis patients. Similarly, both animal and human studies indicate a regulatory role of the Th17 cells in AS; most critical observations are that Th17 cytokines (IL-17 and IL-22) can contribute to bone erosion, osteitis and new bone formation the hall mark skeletal features associated with the pathophysiology of AS. In this review article, we have discussed the contributing role of the IL-23/IL-17 axis in the pathogenesis of PsA and AS.