An emerging role of interleukin-23 in rheumatoid arthritis. (4th March 2019)

• Record Type: Journal Article
• Authors: Yuan, Na; Yu, Guimei; Liu, Di; Wang, Xiancheng; Zhao, Ling
• Is Part Of: Immunopharmacology and immunotoxicology. Volume 41:Number 2(2019)
• Page Start: 185
• Page End: 191
• Publication Date: 2019-03-04
• Subjects: Dendritic cells -- interleukin-17 -- interleukin-12 -- neutralizing antibodies -- osteoclasts; Immunopharmacology -- Periodicals; Immunotoxicology -- Periodicals; Antibody-toxin conjugates -- Periodicals; Immunology -- Periodicals; 615.37
• DOI: 10.1080/08923973.2019.1610429
• Languages: English
• ISSNs: 0892-3973

Abstract

Abstract: Rheumatoid arthritis (RA) is an autoimmune, chronic inflammatory disease and is characterized by destruction of the articular cartilage. A number of pro-inflammatory cytokines work sequentially and in concert with one another to induce the development of RA. IL-23, a member of IL-12 family, is composed of p19 and p40 subunits and it interacts with IL-23 receptor complex to trigger plethora of biochemical actions. A number of preclinical studies have shown the role of IL-23 in the development of RA in rodents. IL-23 receptor signaling is primarily linked to the activation of JAK-STAT, tyrosine kinase 2, NF-kB, and retinoic acid receptor-related orphan receptors. IL-23 produces its osteoclastogenic effects, mainly through IL-17 and Th17 cells suggesting the importance of IL-23/IL-17/Th17 in the joint inflammation and destruction in RA. Monoclonal antibodies targeted against IL-23, including tildrakizumab and guselkumab have been developed and evaluated in clinical trials. However, there are very limited clinical studies regarding the use of IL-23 modulators in RA patients. The present review discusses the different aspects of IL-23 including its structural features, signal transduction pathway, preclinical, and clinical role in RA.