Abstract

English

Highlights

  • The pathogenesis of rheumatoid arthritis (RA) involves systemic dysregulation of T and B lymphocytes resulting in immune responses against self-antigens, and leading to downstream effects such as cartilage destruction, pannus formation, and bone erosion

  • With multiple small-molecule inhibitors being developed to treat chronic inflammation, the future appears promising for an increased variety of treatment options for patients with RA

  • During the multi-step pathogenesis of RA, a host of intracellular signalling kinases are involved in initiation, inflammation, and bone resorption, including Janus kinase 1/3 (JAK1/3) in T cells and, in B cells, spleen tyrosine kinase (SYK) and Bruton’s tyrosine kinase (BTK)

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Summary

Introduction

Rheumatoid arthritis (RA) is a systemic disease characterized by circulating autoantibodies, synovial inflammation, pannus formation, and cartilage and bone destruction in affected joints. During the multi-step pathogenesis of RA, a host of intracellular signalling kinases are involved in initiation, inflammation, and bone resorption, including Janus kinase 1/3 (JAK1/3) in T cells and, in B cells, spleen tyrosine kinase (SYK) and Bruton’s tyrosine kinase (BTK). These mediate cell survival and the inflammatory response[2]. RA has been a disease of interest for tyrosine kinase modulation, with small molecule JAK inhibitors leading the way in this approach to the clinical treatment of patients with RA. This review focuses primarily on inhibitors of the B-cell kinases SYK and BTK that are currently in clinical development

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