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Researchers at VIB and Ghent University have uncovered how an important driver of inflammation is activated at the molecular level. Their findings, published in Science Immunology, also explain how a medicine used to treat a severe form of psoriasis blocks this inflammatory signal.

Inflammation is an essential part of the body's defense against infection and injury. But when inflammatory signals become too strong or poorly controlled, they can contribute to diseases such as psoriasis.

One important player is the IL-36 receptor, a protein that helps cells respond to inflammatory signals. Researchers led by Dr. Danielle Clancy and professor Savvas Savvides (VIB-UGent Center for Inflammation Research) have now revealed in unprecedented detail how this receptor is switched on.

Using the VIB-VUB cryo-electron microscope, which allows scientists to visualize biological molecules at near-atomic resolution, the team captured the molecular machinery assembled around the IL-36 receptor to produce an inflammatory signal.

They discovered a surprising mechanism. An inflammatory molecule called IL-36γ initially attaches relatively weakly to the receptor. But that first contact makes it possible for another receptor component to join much more tightly, creating a stable complex that can trigger a strong inflammatory response.

"You might expect the strongest inflammatory signal to start with the tightest interaction, but that isn't what we see here," says first author Dr. Julie Andries.

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