Effect of interleukin-6, -17, -21, -22, and -23 and STAT3 on signal transduction pathways and their inhibition in autoimmune arthritis.

Rheumatic diseases are complex autoimmune diseases which include among others rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), and psoriatic arthritis (PsA). These diseases are characterized by prolonged and increased secretion of inflammatory factors, eventually leading to inflammation. This is often accompanied by persistent pain and stiffness in the joint and finally bone destruction and osteoporosis. These diseases can occur at any age, regardless of gender or origin. Autoimmune arthritis is admittedly associated with long-term treatment, and discontinuation of medication is associated with unavoidable relapse. Therefore, it is important to detect the disease at an early stage and apply appropriate preventative measures. During inflammation, pro-inflammatory factors such as interleukins (IL)-6, -17, -21, -22, and -23 are secreted, while anti-inflammatory factors including IL-10 are downregulated. Research conducted over the past several years has focused on inhibiting inflammatory pathways and activating anti-inflammatory factors to improve the quality of life of people with rheumatic diseases. The aim of this paper is to review current knowledge on stimulatory and inhibitory pathways involving the signal transducer and activator of transcription 3 (STAT3). STAT3 has been shown to be one of the crucial factors involved in inflammation and is directly linked with other pro-inflammatory factors and thus is a target of current research on rheumatoid diseases.