Researchers Discover Genetic Basis for Eczema

December 21, 2012

New Avenue to Therapies

Eczema or Atopic dermatitis (AD) start with an itchy skin rash, but left untreated, can flare up across the entire body. Most sufferers develop symptoms as infants and it affects millions of adults around the world. There is no cure.

Managing this chronic illness means applying moisturizing lotions and anti-inflammatory corticosteroids, which can have harmful side effects. A team led by Arup Indra, Associate Professor in the Dept. of Pharmaceutical Sciences, College of Pharmacy at OSU/OHSU found that eczema can be triggered by inadequate CTIP2, a protein and master regulator that affects other genetic functions as well. They have identified two ways in which improper function of CTIP2 can lead to eczema.

In a recent publication, they 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 and alters body’s immune responses.

Levels of this inflammatory TSLP, which is ordinarily undetectable in human skin, were found to be 1000 times higher in laboratory animals that had been genetically modified to have no Ctip2 production in skin cells. TSLP overproduction in the AD patients has been a risk factor for the development of allergic airway inflammation and asthma.

The creation of this new research model could be used to screen for drugs with potent anti-inflammatory activities and  may lead to a more effective treatment against  AD, Indra says.


Arup Indra, MD, Associate Professor, Department of Pharmaceutical Sciences, Oregon State University/Oregon Health & Science University.

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