Researchers from Trinity College Dublin have achieved a significant advancement in their knowledge of how inflammation is controlled. They have revealed that a crucial immunological alarm protein thought to suppress the immune response actually has the opposite effect. The findings of the study published in the journal Science Immunology. Their work has numerous potential impacts, especially in the context of understanding and responding to autoimmune disorders and inflammation. While our immune system serves a very important function protecting us from infection and injury, when immune responses become too aggressive this can lead to damaging inflammation, which occurs in conditions such as rheumatoid arthritis and psoriasis. Inflammation is triggered when our bodies produce “alarm proteins” (interleukins), which ramp up our defenses against infection and injury by switching on different components of our immune system. Understanding how and when such alarm proteins are produced and how they activate our immune system has led to major breakthroughs in the treatment of many immune conditions. Now, scientists from the Smurfit Institute of Genetics at Trinity College Dublin, led by Seamus Martin, Smurfit Professor of Genetics, have found that Interleukin-37 has an unexpected function as an immune-activating molecule, as previous studies suggested that this interleukin instead served as an “off switch” for the immune system.