Study: How Psoriasis Plaques Fight Viral Infection
Psoriasis plaques rarely become infected and a new report helps explain why this is the case.
The study, published in Science Translational Medicine, compared psoriasis lesions with atopic dermatitis lesions. While people with atopic dermatitis are vulnerable to infection through the damage caused by skin lesions, those with psoriasis are much less likely to develop infections through the skin damage of their plaques. The report helps explain why this is the case, particularly for viruses.
Type 17 helper T cells, a specific kind of white blood cell, stimulate the release of so-called "antiviral proteins," the authors of the report show through a series of experiments. The cells produce a protein called interleukin 29 (IL-29) that, until now, researchers had not known T cells could produce. IL-29 is one of a large class of molecules known as cytokines that help control the immune system.
Nothing about IL-29 suggests it as a target for psoriasis therapy, said Andrew Johnston, assistant research professor of dermatology at the University of Michigan Medical School, "given that we currently have some excellent targetable cytokines, especially those targeted by drugs that are coming to market soon ." For example, Johnston cited several drugs in Phase III clinical trials that target IL-17. But the findings round out the story of why psoriatic plaques so rarely become infected. The antibacterial and antifungal proteins that are present in plaques are released by signals and cells that researchers already had identified, but for antiviral proteins, researchers did not know the source. "This paper nicely puts everything into place," Johnston said.
October 14, 2013