Neutrophil Extracellular Traps Tied to Rheumatoid Arthritis: Points to Ponder

Abstract

In recent years, neutrophil extracellular traps at the forefront of neutrophil biology have proven to help capture and kill pathogens involved in the inflammatory process. There is growing evidence that persistent neutrophil extracellular traps drive the pathogenesis of autoimmune diseases. In this paper, we summarize the potential of neutrophil extracellular traps to drive the pathogenesis of rheumatoid arthritis and experimental animal models. We also describe the diagnosis and treatment of rheumatoid arthritis in association with neutrophil extracellular traps.

Keywords: anti-citrullinated protein antibodies; autoimmunity; chronic inflammation; citrullinated autoantigens; neutrophil extracellular traps; protein-arginine deiminase type 4; rheumatoid arthritis.

Figure 1

The role of neutrophil extracellular traps (NETs) in the pathogenesis of rheumatoid arthritis (RA). Various elements in the peripheral blood of patients with RA can stimulate NET formation. Excessive NET formation leads to the production of deaminated antigens such as citH2A, citH2B, and citH4 histones. In a joint with RA, presented citrullinated antigens induce antigen-driven autoimmune responses and lead to the generation of anti-NET autoantibodies. Thus, persistent inflammation of the synovial membranes occurs.