What we found was that these kinases that are regulated by calcium actually regulate the strength of activation of STAT1 by the interferons, but they do not regulate the strength of activation of STAT2, said Dr. Ivashkiv. The idea was if you block these signaling pathways, would you block the STAT1 part, which controls the inflammatory/deleterious effects and preserve the antiviral part. We tested that in an animal model of lupus and we were able to show, in vivo, that you can suppress STAT1 activation by inhibiting the calcium-dependent kinases.
The researchers say that their work has identified a new therapeutic approach for attacking lupus. What the companies are trying to develop are, basically, antibodies against the interferons. The concern there is that if you block the interferon completely, patients may become very immunosuppressed and unable to handle viral infections, Dr. Ivashkiv said. Our idea is that if you block these calcium pathways, you could block the deleterious effects of the interferon, but maintain the antiviral effects.
Lupus is an autoimmune disease that can affect various parts of the body, including the skin, joints, heart, lungs, blood, kidneys and brain. Inflammation, considered the primary feature of lupus, is characterized by pain, heat, redness, swelling and loss of function. In most people, the disease affects only a few organs and symptoms are mild, but in others, the disease can cause serious and even life-threatening problems. According to the Lupus Foundation of America, an estimated 16,000 Americans develop lupus each year.
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