Eight out of ten people who brush against poison ivy in their yard or on a hike will pay the price with a painful, itchy rash. But when it comes to stopping the itch, there’s no real foolproof remedy—yet. As Ryan Cross reports for Scientific American, a new study in mice has pinpointed a way to stop the itch from within the tiny creature's molecular pathways, a development that could lead to better treatments against the rash.

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In a new study published in the journal PNAS, researchers describe how they identified the molecular pathway that causes the brain to interpret nerve signals from poison ivy rashes as itchy. The cause appears to be interleukin-33 (IL-33), a protein that regulates inflammation and immune response inside cells and that is associated in humans with itchy skin conditions like psoriasis. To track down the culprit, the team went in search of genes that were transcribed, or copied, at higher levels by mice that had been exposed to poison ivy.

Then, the team went one step further. They developed an antibody against the protein and and its receptor, then gave it to poison ivy-exposed mice. When they did so, the mice showed less inflammation and didn’t scratch themselves as much. Now, according to a release, they’re conducting Phase 1 clinical trials with the antibody on humans to figure out if it’s safe.

The breakthrough could one day help humans better fight the uncomfortable symptoms of an allergy to urushiol. Eighty to ninety percent of adults are allergic to urushiol chemicals, which are found in poison ivy and its relatives, poison sumac and poison oak, and develop a rash when their skin comes into contact with the substance. Although antihistamines and steroids are often prescribed to those with the rash, they don’t really do much for the most severe itching. That’s because “it arises from a different source,” says Sven-Eric Jordt, a Duke University anesthesiologist who was the paper’s senior author, in a release.

Though the study suggests that the source is in fact IL-33, that might not be the case. Animal research often reveals information that can be translated into clinical solutions for humans—but it doesn’t always work. To prove a similar benefit for humans, researchers must first detect the protein in humans with the rash. If they do, better treatments could be around the corner—and people who want to get outside without fearing weeks-long itch attacks could have happier days ahead.