University of Michigan research sheds new light on why certain people are more likely to suffer from rheumatoid arthritis - paving the way to explore new treatments for both arthritis and other autoimmune diseases.
The new UMHS research in mice identifies how a specific group of genes works behind the scenes to activate the bone-destroying cells that cause severe rheumatoid arthritis, a debilitating health issue for millions of Americans.
"We believe this could be a significant breakthrough in our understanding of why certain genes are associated with higher risk of rheumatoid arthritis and other autoimmune diseases - a link that has been a mystery in the field for decades," says lead author Joseph Holoshitz, M.D., professor of internal medicine and associate chief of research in the division of rheumatology at the U-M School of Medicine.
"We hope that this improved understanding will open the door to future design of drugs to treat this crippling disease and autoimmune disease in general."
The research appeared in The Journal of Immunology and was highlighted by Nature Reviews Rheumatology.
Rheumatoid arthritis is a chronic inflammatory disorder that damages the lining of joints and causes bone erosion, joint deformity and disability. The disease is an autoimmune disorder, characterized by the body's immune system mistakenly attacking the body's tissues.
Researchers have long studied the phenomenon of why certain versions of an inherited group of genes known as "human leukocyte antigen" (HLA) are associated with autoimmune disorders. One subset of these HLA genes that codes a protein sequence called "shared epitope" represents the most significant genetic risk factor for rheumatoid arthritis, affecting disease susceptibility and severity. However, until now, the reason for this strong link has been unclear.