The Synovium in Rheumatoid Arthritis



Carol A Hitchon, Hani S El-Gabalawy*
University of Manitoba, Winnipeg, Manitoba, Canada


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© Hitchon and El-Gabalawy; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the University of Manitoba, RR149, 800 Sherbrook Street, Winnipeg, Manitoba, R3A-1M4, Canada; Tel: 204-787-2208; Fax: 204-787-2475; E-mail: elgabalh@cc.umanitoba.ca


Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease targeting multiple joints. The synovium is the primary site of the inflammatory process, which if untreated leads to irreversible damage to the adjacent cartilage and bone. It is now well established that autoantibodies that are characteristic of RA, including rheumatoid factor (RF) and anti-citrulluninated protein antibodies (ACPA), are present before clinical disease onset. Studies in both humans and animal models are beginning to provide new insights into how this asymptomatic autoimmunity evolves into an inflammatory process that is localized in the synovium.

Once RA synovitis established, a number of amplification mechanisms serve to sustain the process leading to the persistence of the disease. These mechanisms include engagement of the resident mesenchymal cells and the establishment of ectopic lymphoid structures in the synovium, although the relationship between these lymphoid structures and the presence of RA autoantibodies remains unclear.

An enhanced understanding of the mechanisms that initiate and sustain RA synovitis offers unprecedented opportunities for therapeutics, and ultimately prevention strategies.

Keywords: Rheumatoid, synovium, innate, lymphoid neogenesis..