Recent insights into the role of autophagy in the pathogenesis of rheumatoid arthritis

Abstract

Autophagy appears to play a dual role in eukaryotic cells. It manifests cytoprotective effects through the regulation of catabolic processes and the clearance of pathogens; however, a correlation between autophagy and the pathogenesis of autoimmune/autoinflammatory conditions has recently been described. Autophagy has emerged as a mediator in the pathogenesis of RA. Autophagy may regulate apoptosis resistance and hyperplasia in synovial fibroblasts, promote osteoclastogenesis and stimulate osteoclast-mediated bone resorption through the delivery of citrullinated peptides to MHC compartments, which results in the activation of the innate and adaptive immune response, thereby resulting in RA. Given the likely importance of autophagy in the pathogenesis of RA, here we reviewed the detailed mechanisms concerning the pathogenicity of autophagy and autophagy proteins in RA.

Keywords: T cells; autophagy; chondrocytes; citrullination peptides; osteoclasts; proinflammatory cytokines; rheumatoid arthritis; synovial fibroblasts.