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Toronto researchers first to discover new genetic clue in the development of rheumatoid arthritis
Date:8/14/2011

ically modified mice in which PTPN22 had been altered to mimic a genetic mutation found in many RA patients. The effects of this change on immune cells were observed in the mice, and the studies were then repeated in human blood samples from patients with and without RA. By this means, the group honed in on the impact of a key protein called Lyp/Pep thatin healthy cellsprevents the hyper-immune responses that lead to autoimmune disorders. The group found that this gene mutation leads to decreased levels of Lyp, thereby removing a natural brake that normally prevents the inflammatory processes underlying RA and many other autoimmune conditions.

"Measuring levels of this protein will help us monitor disease severity in patients with autoimmune disorders, test the effects of various therapies including new drugs, and determine which treatments work best in specific patients," said Dr. Edward Keystone, co-author of the study and Director of the Rebecca MacDonald Centre for Arthritis and Autoimmune Disease at Mount Sinai Hospital. "We are truly seeing genomics in action with this study, and the results give us new hope for improving patient outcomes."

Dr. Keystone emphasized the importance of this type of research to the practice of medicine in general, noting that advances in genetics knowledge are allowing for earlier diagnoses and more personalized treatments that give patients better outcomes.

"Using the powerful genetic tools now available, previously cryptic diseases are being dissected and their underlying causes identified," said Dr. Jim Woodgett, the Lunenfeld's Director of Research. "Drs. Siminovitch and Keystone are at the leading edge of employing these genomic approaches for the benefit of patients, seamlessly combining their research skills with clinical insights."


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Contact: Karin Fleming
fleming@lunenfeld.ca
Samuel Lunenfeld Research Institute
Source:Eurekalert

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