The findings may open the way to new therapies for this frustrating syndrome, known as atopic dermatitis, which is difficult to treat and has no known cure. Eczema is also related to, and can sometimes cause, asthma, a potentially deadly immune dysfunction.
Pharmaceutical scientists at Oregon State University (OSU) found that eczema can be triggered by inadequate Ctip2, a protein and master regulator that affects other genetic functions. They have identified two ways in which Ctip2 can lead to eczema, the journal Public Library of Science ONE reports.
The researchers found that Ctip2 controls lipid biosynthesis in the skin, the fats that are needed to help keep skin healthy and hydrated. In the new study, they discovered that Ctip2 suppresses TSLP, a cytokine protein produced by skin cells that can trigger inflammation, according to an Oregon statement.
Levels of this inflammatory TSLP, which is ordinarily undetectable in human skin, were found to be 1,000 times higher in lab animals that had been genetically modified to have no Ctip2 production in their skin.
"In these studies, we've basically shown that inadequate Ctip2 is reducing the lipids in skin that it needs to stay healthy, protect itself and perform its function," said Arup Indra, associate professor of pharmacy at the OSU College of Pharmacy.
"At the same time this can allow unwanted formation of proteins that trigger inflammation. The skin's ability to resist inflammation is going down just as the amount of inflammation is going up, and the underlying reason is that Ctip2 is not doing its job. Either or both of these problems can lead to eczema," Indra added.
Atopic dermatitis is linked with a dysfunctional immune response, but researchers have never understood the underlying cause.
Existing treatments use moisturizers to try to protect skin, and in difficult cases powerful steroid drugs can help, but they often have significant unwanted side effects when used for a long time.
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