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Trigger for Common Skin Disease Found
An immune molecule that normally assists in cell “suicide†may be an important trigger in the development of the common skin disease psoriasis, according to scientists from the Technion-Israel Institute of Technology and State University of New York, Stony Brook.
The culprit, a molecule called Fas, acts as a middleman between activated immune cells and a handful of inflammatory hormones involved in psoriasis flare-ups, say Technion researcher Dr. Amos Gilhar and colleagues. The study appears in the January, 10 2006 American Journal of Pathology.
Psoriasis is a non-contagious, lifelong skin disease that usually appears as scaly and inflamed patches of skin, although it can take several different forms. In patients with psoriasis, the white blood cells that make up the body’s immune defense system go into overdrive, triggering other immune responses that pile up skin cells at an abnormal rate.
Current treatments for psoriasis such as the drug Enbrel focus on these inflammatory hormones, but the researchers were able to stop the development of psoriasis in mice long before these hormones came into play by injecting an Fas-blocking antibody.
“The finding that antibodies to Fas can prevent psoriasis further demonstrates the complexity of the disease and its numerous molecular pathways,†Gilhar says.
The researchers suspected that the Fas molecule was in the middle of this process, since it is found at high levels in psoriatic skin and leads an intriguing dual life. Most of the time, Fas guides the normal process of cell suicide called apoptosis. But in cells where apoptosis is blocked by other molecules, as it is in psoriatic cells, Fas switches roles and encourages the production of common inflammatory hormones instead.
To figure out exactly where Fas stood in the development of psoriasis, Gilhar and colleagues transferred grafts of clear, non-involved skin from human psoriasis patients to mice. They injected the mice with white blood cells bearing the Fas molecule on their surfaces to jump-start the formation of psoriatic skin lesions.
By blocking Fas action with a special antibody, the researchers were able to show that Fas actually is the key middleman in psoriasis formation. Without Fas, the natural killer cells were unable to trigger the production of the inflammatory hormones that lead to the characteristic skin thickening and other signs of psoriasis.
There is some evidence that Fas is involved in other skin conditions such as eczema, so future treatments targeting the Fas pathway may prove useful for a variety of diseases, suggests Dr. Richard Kalish, Gilhar’s collaborator from SUNY Stony Brook. However, researchers need to develop a human antibody to Fas before the technique could be tested in people.
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Dr. Amos Gilhar , Technion
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