White blood cells fight infection by producing an array of messenger molecules called cytokines, which coordinate the immune system’s counterattack. These molecules may provide new ways to treat autoimmune disease (in which the immune system mistakenly attacks healthy tissue) by blocking only inappropriate responses, leaving the immune system able to defend against infection.
According to two studies in the September Nature Immunology, a cytokine called interleukin 27 (IL-27) controls inflammation of the central nervous system—a feature of several autoimmune disorders, including multiple sclerosis (MS).
One team, led by Christopher Hunter of the University of Pennsylvania’s School of Veterinary Medicine, showed that IL-27 suppresses specific immune cells that cause chronic inflammation through another cytokine, IL-17. When mice lacking the IL-27 receptor were given an experimental infection, they developed severe brain inflammation—while normal mice did not—and showed high levels of the immune cells whose growth IL-27 prevents.
Meanwhile, a group led by Nico Ghilardi of Genentech in South San Francisco found that mice without the IL-27 receptor were more susceptible to experimental autoimmune encephalomyelitis, an MS-like disease. These mice also showed higher levels of IL-17, indicating that IL-27 would normally have countered this cytokine’s inflammatory effects.
“IL-27 was originally thought to cause inflammation, not control it, so these new findings represent an important part of a paradigm shift,” Hunter says. He notes that some cytokine-targeting therapies leave patients vulnerable to opportunistic infections.
“Understanding how molecules like IL-27 modify the immune system could lead to better treatments for autoimmune disease,” he says.