Immune Molecule Is Trigger for Psoriasis

An immune molecule called Fas, which normally assists in "cell suicide,” has a role in psoriasis formation. It acts as an intermediary between activated immune cells and a handful of inflammatory hormones involved in psoriasis flare-ups.

Psoriasis is a non-contagious lifelong skin disease that usually appears as scaly and inflamed patches of skin. In patients with psoriasis, the white blood cells that make up the body's defense system are overactive, triggering other immune responses that pile up skin cells at an abnormal rate.

Researchers were able to block the development of psoriasis in mice by injecting a Fas-blocking antibody. Dr. Amos Gilhar and colleagues from the Technion School of Technology (Haifa, Israel) and Dr. Richard Kalish of the State University of New York at Stony Brook (Stony Brook, NY, USA) 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 induce the formation of psoriatic skin lesions. When they blocked the Fas action with antiFasL or antiFas monoclonal antibody, the natural killer cells were unable to trigger the production of inflammatory hormones that lead to the characteristic thickening and other symptoms of psoriasis. The study appeared in the January, 2006 American Journal of Pathology.

There is some evidence that Fas is involved in other skin conditions such as eczema, but researchers need to develop a human antibody to Fas before the technique can be tested in people.



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