Dr. Johannes M. Weiss and colleagues at the University of Ulm, Ulm, Germany have discovered that osteopontin (OPN) contributes to allergic contact dermatitis.
They present these findings in the January 2010 issue of the American Journal of Pathology.
Allergic contact dermatitis is a hyperreaction of the immune system to either allergens or irritants on the skin, such as poison ivy, nickel, or latex. Contact dermatitis results in large, burning, and itchy rashes, which can take anywhere from several days to weeks to heal. Once allergic contact dermatitis occurs, only strict avoidance can prevent a recurrence, and there is no method to resist persistent sensitization.
Seier et al hypothesized that OPN, an immune mediator that has been shown to worsen the effects of autoimmune disease, played a role in eliciting and facilitating chronic allergic contact dermatitis. They found that both skin cells and immune cells secreted OPN in allergic contact dermatitis lesions. OPN was strongly induced in antigen-specific immune cells in a murine model of chronic contact hypersensitivity, and OPN-deficient mice had a less severe chronic contact hypersensitivity response. As anti-OPN antibody treatment partially suppressed the symptoms of chronic contact hypersensitivity, OPN may serve as a new therapeutic target for allergic contact dermatitis.
Dr. Weiss's group suggests that "[their] data support a model in which OPN has an important function for [immune]-mediated skin inflammation, which may open the perspective to use anti-OPN antibody preparations for the treatment of therapy refractory [immune] cell-mediated skin disease."
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