Commentary: Regulation of autoimmune arthritis by the SHP-1 tyrosine phosphatase

Rheumatoid arthritis (RA) is a systemic autoimmune disease leading primarily to the inflammatory destruction of the synovial joints, ultimately resulting in loss of mobility and a decreased quality of life. Recent advances in RA-related research resulted in the introduction of Janus kinase (JAK) inhibitors to the therapeutic arsenal. JAK inhibitors are orally available and provide efficacy similar to that of disease-modifying anti-rheumatic drugs. However, due to the limited selectivity of these drugs, many RA patients experience adverse effects. The potential benefit of modulating protein tyrosine phosphatases, instead of inhibiting kinases, has not been explored. Using an animal model of RA, our group investigated the role of the Src homology region 2 domain-containing phosphatase 1 (SHP-1) in inflammatory arthritis. The purpose of the present article is to highlight important conclusions of our previous paper entitled “Regulation of autoimmune arthritis by the SHP-1 tyrosine phosphatase”. Herein we briefly present and discuss the observations of this study. We also outline future directions toward investigating the therapeutic potential of targeting SHP-1 in inflammatory arthritis in order to develop a new type of orally available drugs for the treatment of RA.