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Genetic finding suggests alternative treatment strategy for common, complex skin disorders

tional Institutes of Health. "Only by conducting this kind of basic research can we hope to understand the causes of complex diseases. And only by understanding disease can we produce a future in which we can predict who is at risk, pre-empt the illness from ever occurring and personalize the treatment when it does."

Several recent studies have suggested that defects in the skin barrier may be as important to eczema and psoriasis as the hyperactive response of the immune system. In addition, doctors have observed that individuals with eczema are also likely to develop hay fever and asthma, suggesting a common mechanism for both disorders. The other risk factor for these conditions is having a relative with the disorder, suggesting a genetic connection.

To test whether a defective skin barrier can actually produce these diseases, a team of NIH researchers focused on a specific gene called connexin 26, which makes a protein that forms connections between skin cells that create the normal barrier. When the skin is intact, the production of connexin 26 is turned off once there is enough to hook all the skin cells together. When skin is damaged by a cut or a scrape, connexin 26 is produced while new skin cells reproduce and heal the wound. Researchers have shown that connexin 26 production is turned on in the sore skin of people with psoriasis, but it wasn't clear what role connexin 26 played in the disorder.

To determine connexin 26's role in psoriasis, NIH researchers created a line of transgenic mice that over-produce connexin 26. The resulting mice develop psoriatic-type skin sores, just like humans with psoriasis.

"This discovery demonstrates the power of animal models to unravel complex conditions of medical importance," said Eric D. Green, M.D., Ph.D., NHGRI's scientific director and the director of the institute's Division of Intramural Research, where the research was conducted. "Our current abilities to rapidly create new
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Contact: Geoff Spencer
spencerg@mail.nih.gov
301-402-0911
NIH/National Human Genome Research Institute
25-Apr-2006


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