Review Version 1 This version is not peer-reviewed
Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis
Version 1 : Received: 31 July 2021 / Approved: 2 August 2021 / Online: 2 August 2021 (10:52:42 CEST)
How to cite: Kondo, N.; Kuroda, T.; Kobayashi, D. Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis. Preprints 2021, 2021080015 Kondo, N.; Kuroda, T.; Kobayashi, D. Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis. Preprints 2021, 2021080015
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic systemic inflammation causing progressive joint damage that can lead to lifelong disability. The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause damage to both cartilage and bone. Involvement of the cytokines TNF- and IL-6 is central to the pathogenesis of RA, but recent research has revealed that other cytokines such as IL-17, IL-23, GM-CSF, IL-33, and IL-2 also play a role. Clarification of RA pathology has led to the development of therapeutic agents such as biological disease-modifying anti-rheumatic drugs (DMARDs) and Janus kinase (JAK) inhibitors, and further details of the immunological background to RA are emerging. This review covers existing knowledge regarding the roles of cytokines, related immune cells and the immune system in RA, manipulation of which may offer the potential for even safer and more effective treatments in the future.
Rheumatoid arthritis; TNF-; IL-6; IL-17; IL-23; GM-CSF; IL-33; IL-2
LIFE SCIENCES, Biochemistry
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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