IL-6, IL-12, IL-15 and IL-23 Expression Levels in Rheumatoid Arthritis Patients

Rheumatoid Arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation and articular damage.

Continuous medical research has dramatically improved the outcomes for patients with RA. Traditional therapeutic approaches have relied on glucocorticoids, nonsteroidal anti-inflammatory drugs (NSAIDs) and disease modifying antirheumatic drugs (DMARDs) such as methotrexate, sulfasalazine or leflunomide. Glucocorticoids and NSAIDs interfere with the inflammatory cascades while DMARDs impede both the inflammatory and the destructive processes of RA.

These drugs, although efficient, are not specifically directed against inflammatory cells or cytokines and are associated with significant toxicity. The development of biologic DMARDs (bDMARDs), has been an important step forward. Their ability to neutralize specific cytokines or target distinct immune cells filled a gap in existing treatment options for RA. [3]. However, some patients still have only partial or no response to bDMARDs. More recently, a group of drugs has been developed that inhibit the janus kinase (JAK) family of intracellular tyrosine kinases, which transmit cytokine- mediated signals via the JAK-signal transducer and activator of transcription (STAT) pathway [4]. Baricitinib, with a selectivity to inhibit JAK1 and 2, has been FDA approved for RA in 2018 [5].

Many cytokines such IL-6, IL-12, IL-15, IL-23, (GM-CSF) and (IFNs) are associated with the pathogenesis of RA. These cytokines transduce signals via the JAK-STAT pathway.