A new study published in the December issue of Arthritis and Rheumatism says that a protein called Type II Collagen (CII) could have a vital role in the pathogenesis of rheumatoid arthritis (RA), a very painful inflammatory joint condition.
This protein was found by a team of researchers at the Queen Mary's School of Medicine and Dentistry at the University of London. It appears that the protein modifies itself and then proceeds to systematically destroy the body's immune system and concurrently increases inflammation of the joints. These findings could be a pointer towards the development of new drugs to combat the disease.
Type II Collagen (CII) is a major protein found abundantly in cartilage, bone and tendons. The team felt that CII could trigger RA when it is stressed by inflammation. They say that when inflammatory cells enter normal tissue they tend to overuse the oxygen supply. This means that proteins are deprived of this vital element and consequently undergo some modification. To prove this point they took blood samples from 31 male and female RA patients and from 41 patients who had other inflammatory conditions like osteoporosis, back pain and gout. All of these samples were subjected to exposure by CII protein taken from cows as well as a modified CII. This is typically present in rheumatic inflammation. The researchers found that CII did not bind in the blood samples of RA patients. But 45 percent of the RA blood samples formed immune complexes with the altered form of the protein. The researchers say that CII serves to accelerate and already worse condition in RA. "Our study has important implications for the further study and enhanced understanding of the pathology of RA," said study author Ahuva Nissim. "In the future, understanding of this process will help us develop specific therapeutics which will target only the inflamed joints."