Study sheds new light on this critical proteins involvement in autoimmunity and chronic, corrosive joint inflammation
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of the joints, which gradually erodes the cartilage and bone. The agents of destruction include inflammatory cells, cytokines, and protein-degrading enzymes known as matrix metalloproteinases (MMPs). The vicious cycle begins when inflammatory cells infiltrate the tissue lining the joints and consume excess oxygen. In addition to unleashing MMPs, the oxidative stress provokes non-enzymatic glycation – a chemical binding of sugar molecules and proteins. Telltale signs of glycation have been found in blood, urine, and synovial fluid of RA patients.
The primary protein in cartilage, Type II Collagen (CII) is crucial to joint health and function. Yet, the involvement of CII in the process of joint inflammation has proven difficult to substantiate. To gain a clearer understanding of CIIs role in the pathogenesis of RA, researchers at Queen Mary, University of London and others studied its behavior within an inflamed joint, when modified by oxidants linked to inflammation or by ribose, a five-carbon sugar common to all living cells. Featured in the December 2005 issue of Arthritis & Rheumatism, their findings support CIIs potential contribution to antibody binding and RAs devastating progression.
Amy Molnar | EurekAlert!
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