It can be a relief to scratch the occasional itch, but when itch gets out of control, it can become a serious health problem. How does the body know when to stop?
Scientists at UC San Francisco are getting close to an answer. In a breakthrough that could transform how doctors treat conditions from eczema to allergies, they have discovered a feedback loop centered on a single immune protein called IL-31 that both causes the urge to itch and dials back nearby inflammation.
The findings, published on October 13th in Science Immunology, lay the groundwork for a new generation of drugs that interact more intelligently with the body's innate ability to self-regulate.
Previous approaches suggested that IL-31 signals itch and promotes skin inflammation. But the UCSF team discovered that nerve cells, or neurons, that respond to IL-31, triggering a scratch, also prevent immune cells from overreacting and causing more widespread irritation.
"We tend to think that immune proteins like IL-31 help immune cells talk to one another, but here, when IL-31 talks to neurons, the neurons talk right back," said Marlys Fassett, M.D., Ph.D., UCSF professor of dermatology and lead author of the study. "It's the first time we've seen the nervous system directly tamp down an allergic response."
The discovery could eventually change how asthma, Crohn's and other inflammatory diseases are treated, due to IL-31's presence throughout the body.
"IL-31 causes itch in the skin, but it's also in the lung and in the gut," said Mark Ansel, Ph.D., UCSF professor of immunology and senior author of the study. "We now have a new lead for fighting the many diseases involving both the immune and nervous systems."
More than an itch
sources-science daily
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