New study sheds light on role of type II collagen in rheumatoid arthritis

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Rheumatoid arthritis (RA) is an autoimmune disease which gradually erodes cartilage and bone and is characterised by chronic inflammation of the joints.

RA is triggered when inflammatory cells infiltrate the tissue lining the joints and consume excess oxygen, producing oxidant compounds. The primary protein in cartilage, Type II Collagen (CII), is crucial to joint health and function; yet until recently, its involvement in the process of joint inflammation has proven difficult to substantiate.

To gain a clearer understanding of the role of Type II Collagen in the pathogenesis of RA, researchers at Queen Mary, University of London and others, have studied whether antibodies in RA patients recognise natural or oxidised CII.

The researchers collected blood serum samples from 31 RA patients between the ages of 65 and 93 years, suffering varying stages of the disease and receiving different treatments. For control purposes, serum samples were also collected from 41 patients with other inflammatory joint diseases, including osteoarthritis and lupus, as well as back pain, osteoporosis, and gout.

Both RA and non-RA samples were analysed for their ability to bind to two types of Collagen; a pure and natural CII (obtained from bovine cartilage), and a CII that had been chemically modified to include three oxidant compounds, which are present in a rheumatic joint.

Featured in the December 2005 issue of Arthritis & Rheumatism, their findings support the potential contribution of CII to antibody binding and the devastating progression of rheumatoid arthritis.

Of the 31 RA serum samples analysed, only three showed antibody binding to the natural CII - suggesting the protein is an innocent bystander in autoimmunity and its inflammatory toll on the joints.

However, the percentage of samples that exhibited antibody binding increased four-fold when tested with the chemically modified CII. In fact, 45 per cent of all RA samples showed moderate to strong antibody binding reactions. In contrast, only 1 non-RA sample showed strong antibody binding to the chemically modified CII.

“The present findings support the idea that chemical modification of our body proteins during an inflammatory reaction, in RA in particular and in other diseases in general, is the cause for the chronic nature of autoimmunity,” reflects the study’s leading author, Dr Ahuva Nissim, of Queen Mary’s William Harvey Research Institute. “We propose that the oxidative modification of CII creates a new target for the immune system in RA.”

This hypothesis has important implications for the further study and enhanced understanding of the pathology of RA - a complex autoimmune disease.

The study was a collaboration between researchers at Queen Mary, University of London, King’s College London and the University of Exeter.

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