Illinois Institute of Technology Researchers Discover Antibody Is Plausible Mechanism for How Rheumatoid Arthritis Starts

Antibiglycan Decomposes Collagen Fibers; Results Published in PLoS ONE This Week


Chicago, IL — March 13, 2012 —

Joseph Orgel, associate professor of biology and biomedical engineering at Illinois Institute of Technology, and research assistant professor of biology Olga Antipova published the results of their research that shows a plausible cause of rheumatoid arthritis: the Biglycan antibody. Orgel and Antipova found that an antibody against a molecule (called a proteoglycan) that binds collagen fibrils causes the tissue to fall apart. This mechanism might be analogous to what happens in rheumatoid arthritis. Their results are published March 13 in an article in PLoS ONE, “Non-enzymatic decomposition of collagen fibers by a Biglycan antibody and a plausible mechanism for rheumatoid arthritis.”

“The antibody and only the antibody caused the tissue to disintegrate, not the action of cells or enzymes” said the authors Antipova and Orgel. “This has given us insight into what may be happening in initial stages of rheumatoid arthritis. If we’re right, this understanding could ultimately lead to treatment by countering the interaction of this (autoimmune) antibody with collagen fibers.”

Rheumatoid arthritis is an autoimmune disease – the body’s immune system mistakenly attacks healthy tissue – that causes inflammation in joints and sometimes organs, such as lungs and eyes. It affects more than 60 million people globally, but its cause had been a mystery. “Biglycan antibodies have been detected at the early stages of rheumatoid arthritis and may be considered early RA markers; however, they were never expected to play such a destructive role in cartilage deformation” said Antipova.

The researchers did studies with lamprey (a cartilaginous fish related to hagfish and eels) tissue, then bovine and human tissues, and got comparable results, Orgel added.

“What is exciting is not only the mechanism for rheumatoid arthritis that we describe, but also the fact that it has never before been observed that antibodies can damage tissue directly. It was always assumed to be antibodies associated as markers for cells or enzymes that attacked the tissue.”

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