AB0691 Metformin therapy can restore the balance of TH17 and treg cells in patients with spondyloarthrit

Background Spondyloarthrit (SpA) is a chronic autoimmune disease and is associated with immunological function disorder. Previous studies have observed that increased number of T17 cells and decreased number of Regulatory T (Treg) cell in patients with S [1,2]. However, the current therapy for SpA, focusedon NSAID, biological agents and glucocorticoid, can9t correct the imbalance of Th17 and Treg cells. Metformin has been demonstrated a reducing effect on Th17 cells but an increasing effect on Treg cells, regulating the Thl7/Treg ratio [3]. Objectives The study is to explore the effect of metformin therapy on the balance of Th17 and Treg cells in patients with SpA. Methods SpA patients (n=27) (from August 1st to November 30th in 2016, both outpatients and inpatients in our department, according to American-European Consensus Group criteria for SpA), who were given metformin (750mg/day for 6 weeks). Laboratory indicators were compared before and after metformin treatment. Results The number of Treg cells [25.37 (18.31,45.78) vs.34.43 (25.91,50.31), P=0.015] significantly increased after the treatment. At the same time, there was a significantly decrease in the ratio of Th17/Treg cells [0.26 (0.15,0.48) vs. 0.22 (0.1,0.33), P+0.037]. Besides, Th17 cells were also decreased [7.85 (4.95,10.65) vs. 6.42 (3.7,10.63)]. Conclusions Metformin can restore and maintain the balance of Th17 and Treg cells in the patients with SpA. And it may be a potential therapy for SpA. References Jandus C, Bioley G, Rivals JP, Dudler J, Speiser D, Romero P. Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritides.Arthritis Rheum. 2008;58:2307–17. Shen H, Goodall JC, Hill Gaston JS. Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis.Arthritis Rheum. 2009;60:1647–56. Son HJ, Lee J. Metformin attenuates experimental autoimmune arthritis through reciprocal regulation of Th17/Treg balance and osteoclastogenesis. Mediators Inflamm.2014,2014:973986. Disclosure of Interest None declared