Th17 cells are known to be involved in the pathogenesis several autoimmune conditions including psoriasis and juvenile idiopathic arthritis, JIA. The blockade of IL-17 and or IL-23 are being increasingly considered as therapeutic options in autoimmune arthritis. In juvenile idiopathic arthritis (JIA) we have previously shown that the frequency of Th17 cells is correlated with severity of arthritis, and reciprocally related to the frequency to regulatory T cells (Treg) at the disease site. We have also shown that the lectin like receptor CD161 is expressed both on Th17 cells, but also on a subset of Th1 cells, and a proportion of Treg cells, in the joint. Th1 – like cells in the joints of patients with JIA include a large CD161+ population. Interestingly, Treg which express CD161, also make cytokines including IL-17 and IFNg. When synovial Th17 effector cells undergo plasticity in the joint, they convert to poly-functional cytokine producers, and these “ex-Th17” cells then produce GMCSF in addition to the typical Th1 cytokines. These cells retain their expression of CD161 on their surface. We have now undertaken an extensive molecular analysis of the CD161 +ve and – ve cell populations. In this talk we will consider the lineage, transcriptional and functional relationships between Treg, Th17 and Th1 cells in JIA and the translational implications of these findings.
Disclosure of Interest None declared