An international team led by researchers at UCLA’s Henry Samueli School of Engineering and Applied Science and California NanoSystems Institute has identified an unexpectedly general set of rules that determine which molecules can cause the immune system to become vulnerable to the autoimmune disorders lupus and psoriasis. The breakthrough could lead to new ways of treating the disorders. Researchers discovered that LL37 molecules play an important but unexpected role in revving up the body's self-defense response by organizing self-DNA into periodic lattices that amplify inflammation through innate receptors. A key to triggering the immune response is that the molecules must arrange the DNA so that the receptors bind to them strongly.
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