Objective: This study aims to provide consolidation of current research findings as well
as the most important concepts regarding neutrophil extracellular traps (NETs) in rheumatoid arthritis.
Data Sources: Relevant publications from 2004 to 2018 were identified using PubMed, Web of
Science, Scopus, and eLibrary databases. Primary search terms used were “neutrophil extracellular
traps” or “NETs” in combination with “rheumatoid arthritis”.
Data Synthesis: NETs are distinctive structures promoting capture and non-phagocytic cleavage of
foreign substances. NETs usually consist of thin chromatin fibers decorated with various molecules
of granular, cytosolic, and cytoskeletal origin. NETosis can develop in two ways: either with neutrophil
death or when the viability of the cell prolongs. ROS generation and pronounced protein citrullination
are essential during the initial phase of NETs formation. NETosis is considered to have
certain immunological consequences, including DAMPs-mediated signalling, proinflammatory cytokine
secretion, and contact of extensively modified self and foreign epitopes with antigen-presenting
cells. There are several putative pathogenetic links between NETosis, citrullination, neoepitope
formation, and production of anticitrullined autoantibodies that can strongly influence rheumatoid
arthritis progression. NET-induced vascular injury in rheumatoid arthritis can arise directly from
NETs and indirectly through enhanced thrombosis and atherosclerosis.
Conclusion: NETs are currently estimated as a possible influential factor of rheumatoid arthritis
initiation and/or progression, especially in the context of vascular involvement. NETs can also
serve as a source of novel antigenic biomarkers for the diagnosis of rheumatoid arthritis.