Most of us know the sweet relief of scratching an itch. But when scratching becomes constant, it’s more than annoying—it can turn into a serious health issue. So, what stops the body from itching itself raw?
Researchers at UC San Francisco may finally have an answer. In findings that could shake up how we treat conditions like eczema and allergies, scientists have zeroed in on a single immune protein, IL-31. This molecule doesn’t just trigger the urge to itch—it also throws a wet blanket on nearby inflammation, creating a fascinating feedback loop.
The big reveal, published October 13th in Science Immunology, opens the door for more innovative drugs that harness the body’s own ability to keep itself in check.
For years, scientists thought IL-31 was just a double-trouble signal—causing us to scratch and inflame the skin at the same time. But the UCSF team found something surprising: when neurons sense IL-31 and make us scratch, they also send a signal that reins in immune cells. So, the very pathway that makes you want to itch is also working overtime to prevent your skin from going haywire.
“Usually we think immune proteins like IL-31 are just for immune cells to talk amongst themselves,” said Dr. Marlys Fassett, the study’s lead author. “But here, when IL-31 talks to neurons, those neurons actually talk back—calming the immune system down. We’ve never seen the nervous system step in like this before.”
This new understanding could have implications way beyond itchy skin. IL-31 isn’t just found in the skin—it’s all over the body, in the lungs and gut too. Diseases like asthma, Crohn’s, and other inflammatory conditions could all be affected.
“IL-31 is the ringleader of itch in the skin, but it’s working its magic elsewhere too,” said Dr. Mark Ansel, senior author. “We finally have a clue to why the immune and nervous systems keep crossing paths.”
A deeper dive into "itch cytokines."
IL-31 is part of a group of molecules known for causing itch—cutely nicknamed “itch cytokines.” Fassett, who spends her days both seeing patients and doing research, couldn’t let go of the question: why does the body bother with itchy signals at all? She joined up with Ansel, an expert on asthma, to find out.
Their first move was to knock out the IL-31 gene in mice and hit them with dust mites—a classic trigger for allergies and itching. No IL-31 meant they didn’t scratch. Mission accomplished, right? Actually, no. The researchers saw more inflammation than ever before.
That seemed backwards. Why was there all this inflammation, but no itching? Without IL-31, immune cells go into battle mode with nothing to hold them back. IL-31 was acting as both a troublemaker and a peacekeeper.
Hitting the brakes on inflammation
Digging deeper, the team traced the action to nerve cells in the skin. These neurons, wired to respond to IL-31, did more than urge scratching. They released a signal called CGRP, which actually cooled down the immune response. Knock out IL-31, and you lose that balancing force. The immune response spirals.
Real-world evidence supports the lab findings. Nemolizumab, a drug that blocks IL-31, can clear up eczema’s dry, patchy skin—yet some patients end up trading one skin problem for another, including unexpected lung issues. “Blocking IL-31 across the whole body messes with the feedback system,” Ansel explained. “You take the brakes off, and allergic reactions can start popping up everywhere.”
This discovery flips the old script about what nerves do in allergies. “We used to think nerves just pass along symptoms,” Fassett said. “Now it turns out they’re helping control how bad those symptoms get. If we design treatments that respect this system, we might finally help patients who get flare-ups from ‘itch’ drugs.”
As for what comes next? Fassett has started her own lab at UCSF to unravel these mysteries, while Ansel is chasing down new roles for IL-31 in places where itching doesn’t even happen—like the lungs and gut.
“You don’t feel an itch in your lungs, but IL-31 is definitely doing something there,” Ansel said. “There’s a huge frontier ahead of us, and if we figure it out, the payoff for patients with allergic diseases could be enormous.”
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