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

genetically altered animal models allow researchers to move from conception of an idea to its implementation at an incredible pace."

The discovery broadens the basic understanding of the causes of skin disorders such as psoriasis and eczema, and may well contribute to the basic understanding of asthma and hay fever, conditions that arise when allergens penetrate the tissue barrier in the lungs and nose, respectively.

"Hopefully, this will help us understand the complex genetics of psoriasis," said Julia A. Segre, Ph.D., an investigator in NHGRI's Genetics and Molecular Biology Branch and the senior author on the paper. "Previous genetic studies have focused on the genes that regulate immune response. We are now examining the effect of genes that are involved in both regulating the growth of skin cells and signaling to the immune cells."

The problem causing these related disorders may simply be the body over-reacting to an allergen getting through the barrier that is supposed to block it. "The skin goes into a stress response and overcompensates by trying to rebuild the barrier too fast, actually becoming less effective," Dr. Segre said. "The skin cells grow so fast that they fail to make a normal barrier, and the body is stimulating the immune response because of material (chemicals and allergens) coming through the barrier."

Understanding the genetics of skin disorders may well have important implications for more serious illnesses, such as asthma. It is not uncommon for a family doctor to face the dilemma of a child who has eczema and then having to decide how aggressively to treat the disease. Eczema is not particularly dangerous, but children presenting with eczema commonly go on to develop asthma, which severely compromises quality of life and in rare cases can be lethal. Treating eczema with immune-suppressing drugs, which may also prevent asthma from developing, may cause undesirable side effects.

The genetic stud
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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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