Inflammation helps us repair injuries and defeat infections. It’s supposed to shut down once a crisis is over. In people with lupus, however, inflammation persists and can damage the joints, skin, and organs. Researchers have discovered a molecular sensor in cells known as the NLRP3 inflammasome that triggers inflammation. When the inflammasome detects signs of an injury or infection, it partially switches on. But much like how you can’t access your e-mail with only your username, the inflammasome doesn’t fully activate to begin inducing inflammation until it receives a second type of stimulation–the equivalent of your e-mail password.
Now, Lupus Research Alliance Novel Research Grant recipient Michael Karin, PhD of the University of California, San Diego, and colleagues have uncovered this second trigger. By studying immune cells that promote inflammation, the researchers found that a protein called CMPK2 allows the NLRP3 inflammasome to turn on all the way. In cells that lack the protein, the inflammasome remains off. According to Dr. Karin, researchers should be able to develop drugs to block CMPK2 that could provide a new way to shut off inflammation in patients with lupus. He and his colleagues published their results in the journal Nature.