UCSF Team Identifies Two Key Molecules In Asthma; Important Finding For New Therapies That Treat Disease At Cell Level

Researchers at the University of California San Francisco have identified two molecules that cause cells to cause asthma--a finding that paves the way for developing more effective drugs for treatment.

The molecules connect with a specific cell receptor to alter cellular structure and set up the mechanism of disease.

"It's like finding the words that connect with the ear that enable the process of hearing to be set in motion. Now we can direct further research into how to manipulate these molecules at the outset to change the outcome of the disease," said David B. Corry, MD, an assistant professor of medicine with the UCSF Lung Biology Center at San Francisco General Hospital Medical Center.

Corry is senior investigator of the study, which is reported in the current issue (December 18) of Science. Scientists nationwide have long focused on trying to understand asthma at the cellular level, and the finding is viewed as a significant breakthrough.

The UCSF researchers conducted the study in a mouse model that mimics human asthma.

The team found that disease begins with the presence in lung tissue of two molecules, interleukin-4 and interleukin-13, which then link up with a certain receptor, named the IL-4 receptor alpha. The molecules are hormone-like substances, called cytokines, produced by CD4+ T cells. The receptor is on the surface of these cells and of cells that make up the lung tissue. CD4 cells are the cells that coordinate the overall action of the human immune system, and cytokines modulate this activity.

It is not known why some people have the two molecules--which are known by the shorthand names of IL-4 and IL-13--in their lungs, but it believed to be linked to a genetic predisposition, Corry said.

"The striking message in the scientific investigation is that all the complexity of asthma as a disease comes down to these three elements: molecule, molecule, receptor," Corry added. The

Contact: Corinna Kaarlela
University of California - San Francisco

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