Sven-Eric Jordt, Ph.D.
An NIEHS grantee and colleagues found that the immune system protein interleukin 33 (IL-33) plays a key role in triggering itch from poison ivy, the most common allergic reaction in the U.S. The new findings could lead to treatments for people allergic to urushiol, the oily sap found in poison ivy, poison sumac, and poison oak.
The researchers developed a mouse model that mimicked the skin inflammation and severe itching found in people allergic to poison ivy. Microarray analysis showed that the skin of these mice exhibited high gene expression levels of IL-33 after exposure to urushiol. The researchers then tried blocking IL-33 in the skin using an antibody that stops the processes that communicate itchy skin to the brain. Not only did the antibody reduce inflammation, but it also reduced scratching in mice with poison ivy rashes. The researchers also found they could stop the itch by blocking a receptor for IL-33, called ST2.
Although it was already known that IL-33 can induce inflammation, the new experiments showed that the protein also acts directly on nerves in the skin, exciting them and communicating the itch to the brain. These findings suggest a possible alternative therapeutic approach to the current treatments of antihistamines, which typically don’t stop itch, and corticosteroids, which come with side effects and must be administered soon after the exposure.
Citation: Liu B, Tai Y, Achanta S, Kaelberer MM, Caceres AI, Shao X, Fang J, Jordt SE. 2016. IL-33/ST2 signaling excites sensory neurons and mediates itch response in a mouse model of poison ivy contact allergy. Proc Natl Acad Sci U S A 113(47):E7572-E7579.