PHILADELPHIA The same signal responsible for promoting the type of immune responses that cause asthma and allergy can also limit the type of inflammation associated with debilitating diseases like inflammatory bowel disease, arthritis and multiple sclerosis, according to researchers from the University of Pennsylvania School of Veterinary Medicine. The researchers discovered how IL-25, a signaling protein known as a cytokine, both prevents destructive inflammation and promotes immune responses associated with asthma and allergic responses.

The findings, which appear the April issue of the Journal of Experimental Medicine, suggest that manipulating IL-25 could provide a method to treat a wide variety of chronic inflammatory diseases.

"It appears that IL-25 has a Jekyll and Hyde personality: it can be helpful or hurtful depending on how it interacts with T helper cells, a subset of immune cells that influences inflammatory responses," said David Artis, an assistant professor in Penn's Department of Pathobiology and senior author of the study. "These studies show that IL-25 promotes type 2 T helper cells that drive the type of response required for eradicating worm infections and causing asthma. Importantly, IL-25 can simultaneously limit destructive inflammation caused by inflammatory T helper cells commonly found in diseases like inflammatory bowel disease, arthritis and MS."

IL-25 can be considered a "good" cytokine by limiting chronic inflammatory responses. At the same time, the ability of IL-25 to promote type 2 responses that drive asthma could be considered the "evil" side of the cytokine.

By examining mice infected with Trichuris, a species of intestinal parasites known as whipworms, the researchers were able to define IL-25's role in promoting type 2 inflammation to fight infection. In mice that lack the ability to produce IL-25, researchers saw a dramatic reduction in the ability to mount a type 2 response that eradica
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Contact: Greg Lester
glester@pobox.upenn.edu
215-573-6604
University of Pennsylvania
10-Apr-2006

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