Two immune system proteins could be the culprit behind many lupus patients' resistance to widely used steroid treatments, scientists with the Baylor Research Institute (BRI) in Dallas announced today. It is estimated that more than 5 million people suffer from lupus worldwide.
Currently, those with lupus and other autoimmune diseases, commonly treat the condition with corticosteroids to suppress their overactive immune system and prevent it from attacking healthy tissues which can result in symptoms such as inflammation, pain and organ damage.
These steroid treatments work by killing certain immune system cells, including plasmacytoid dendritic cells (PDCs) that overproduce type 1 interferons, an immune system substance that contributes to lupus and other autoimmune diseases. However, unlike other conditions, steroid treatments are not as effective against these cells in those with lupus.
By largely studying children with systemic lupus erythematosus (SLE), BRI scientists in collaboration with scientists at Dynavax in Berkeley, CA, were able to solve the mystery behind the resistance. They determined that two immune system proteins known as toll-receptor 7 (TLR7) and toll-receptor 9 (TLR9), cause an activation of PDCs the very cells steroids target negating the effects of treatment. BRI scientists reported their findings in the June issue of the journal Nature.
"We have long known that these receptors played a critical role in lupus, but until now, we didn't know they were directly interfering with the effects of steroid treatments," says Virginia Pascual, M.D., one of the principal investigators of the study and a researcher at Baylor Institute for Immunology Research, a component of BRI. "By blocking TLR7 and TLR9 function, we may have found a safer way to treat this debilitating disease."
http://www.medicalnewstoday.com/articles/194474.phpTTT
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