May 20, 2015 08:48 PM
(This post was last modified: May 20, 2015 08:52 PM by Magical Realist.)
"Researchers at the La Jolla Institute for Allergy and Immunology, in collaboration with colleagues the University of California, San Diego, identified a novel drug target for the treatment of rheumatoid arthritis that focuses on the cells that are directly responsible for the cartilage damage in affected joints.
Their findings, published in the May 20, 2015 issue of Science Translational Medicine, could open the door to an entirely new class of medications that specifically prevents joint damage and brings relief to patients who don't respond to available treatment regimes.
Current rheumatoid arthritis treatments focus on intercepting the immune system's misdirected attack on the lining of affected joints to alleviate the debilitating symptoms, reduce inflammation and slow the progression of the disease. "Unfortunately, for around 40 percent of patients,
immune-targeted therapies are not sufficient to bring them into full remission," says the study's lead author Nunzio Bottini, M.D. Ph.D., associate professor at La Jolla Institute and associate professor of Medicine at the University of California, San Diego. "If we could add a drug that acts on a different target without increasing immune suppression it could be very valuable."
Rheumatoid arthritis, an autoimmune disease that leads to stiff, deformed joints and often crippling pain, affects around 1.5 million adults in the United States. The immune system's attack on the body's own tissue leads to chronic, painful inflammation in the affected joints. The inflammatory processes also activate fibroblast-like synoviocytes (FLS), specialized cells that line the inside of joints providing lubrication and repairing joint injuries. Once mobilized, however, the formerly quiescent FLS invade the surrounding cartilage and secrete enzymes that break down the firm, rubbery tissue that cushions the bone. In addition, they trigger bone destruction.
"Even if your inflammation is completely under control with the help of current therapies -- and they are excellent -- the damage to the skeletal structure is not necessarily arrested in the long term because synoviocytes continue to cause damage," explains Bottini. "And although synoviocytes are considered the main effectors of cartilage damage in rheumatoid arthritis there's no therapy directed against them."-------http://www.sciencedaily.com/
Their findings, published in the May 20, 2015 issue of Science Translational Medicine, could open the door to an entirely new class of medications that specifically prevents joint damage and brings relief to patients who don't respond to available treatment regimes.
Current rheumatoid arthritis treatments focus on intercepting the immune system's misdirected attack on the lining of affected joints to alleviate the debilitating symptoms, reduce inflammation and slow the progression of the disease. "Unfortunately, for around 40 percent of patients,
immune-targeted therapies are not sufficient to bring them into full remission," says the study's lead author Nunzio Bottini, M.D. Ph.D., associate professor at La Jolla Institute and associate professor of Medicine at the University of California, San Diego. "If we could add a drug that acts on a different target without increasing immune suppression it could be very valuable."
Rheumatoid arthritis, an autoimmune disease that leads to stiff, deformed joints and often crippling pain, affects around 1.5 million adults in the United States. The immune system's attack on the body's own tissue leads to chronic, painful inflammation in the affected joints. The inflammatory processes also activate fibroblast-like synoviocytes (FLS), specialized cells that line the inside of joints providing lubrication and repairing joint injuries. Once mobilized, however, the formerly quiescent FLS invade the surrounding cartilage and secrete enzymes that break down the firm, rubbery tissue that cushions the bone. In addition, they trigger bone destruction.
"Even if your inflammation is completely under control with the help of current therapies -- and they are excellent -- the damage to the skeletal structure is not necessarily arrested in the long term because synoviocytes continue to cause damage," explains Bottini. "And although synoviocytes are considered the main effectors of cartilage damage in rheumatoid arthritis there's no therapy directed against them."-------http://www.sciencedaily.com/