The gut, skin and lungs act as critical barriers against pathogens and harmful substances. A chemical messenger called IL-22 is one of the key tools your immune system uses to keep those barriers strong, repair them when damaged and call in help when germs invade. But too little IL-22 means infections can break through, and too much can lead to disorders like psoriasis, inflammatory bowel disease, rheumatoid arthritis and even cancer by fueling chronic inflammation.
Effective drugs exist to block IL-23, an upstream signal that tells immune cells to crank out IL-22, but they work broadly and can make patients more vulnerable to infection.
A team of scientists led by Eugene Oltz, PhD, professor and Chair of the Department of Microbial Infection and Immunity at The Ohio State University College of Medicine, worked with colleagues at Washington University School of Medicine and the University of Pennsylvania’s Perelman School of Medicine, to identify the genetic "switches" inside immune cells that turn IL-22 on in different types of immune cells.
Their findings, titled “Cell Type-specific Enhancers Regulate IL-22 Expression in Innate and Adaptive Type 3 Lymphoid Cells,” were just published in Nature Communications. Dr. Oltz says they used a powerful gene-editing technique called CRISPR, to discover two different switches — small stretches of DNA they named E22-1 and E22-2 — that work like dimmer knobs to set IL-22 levels. The study revealed:
Overall, the work could lead to more precise ways to control IL-22 in chronic inflammation, autoimmune disease, infection and cancer by reducing harmful immune overactivity while keeping enough protection against germs.
