Damaging an overactive immune system

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PENNSYLVANIA
BRCA the family of DNA-repair proteins associated with different kinds of cancers including breast, ovarian prostate, and pancreatic interacts with a multipart, molecular complex that is also responsible for regulating the immune system. When certain players in this pathway go awry, autoimmune disorders, like lupus, can arise. Now, researchers in the Perelman School of Medicine at the University of Pennsylvania and colleagues at the University of Leeds, United Kingdom, have deciphered the structure of the complex and have found new molecular targets for fighting autoimmunity. Their findings are published this week in Nature. “The important association between this complex and the immune system originally came about because my lab focuses on how BRCA1/2 function in DNA damage responses, and we realized that immune signaling entailed similar events that are governed by some of the same players involved in BRCA function, said co-senior author Roger Greenberg, MD, PhD, a professor of Cancer Biology and director of Basic Science at the Basser Center for BRCA. An enzyme that functions with BRCA1 to repair damaged DNA also exists within a separate complex called BRISC to regulate immune signaling. Greenberg’s team explored the relationship between BRISC and immune cell surface receptors to better understand the symptoms of lupus and other autoimmune diseases. The overproduction of immune cells, and their signaling compounds called cytokines, stirs up hyper-inflammation that can cause substantial tissue damage, an effect of many autoimmune disorders. Lupus patients, in particular, produce too much of the cytokine interferon, a natural chemical that signals to the immune system in ways that can exacerbate inflammation.— VoM

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