A Polygenic Mouse Model of Psoriasiform Skin Disease in CD18-Deficient Mice

    Daniel C. Bullard, Karin Scharffetter‐­Kochanek, Mark J. McArthur, John G. Chosay, Mollie E. McBride, Charles A. Montgomery, Arthur L. Beaudet
    TLDR CD18-deficient mice developed psoriasis-like skin disease, useful for studying inflammatory skin disorders.
    Researchers generated a hypomorphic mutation in CD18 in mice, leading to increased neutrophil counts and inflammatory defects. When backcrossed onto the PL/J strain, nearly all homozygous mice developed a chronic inflammatory skin disease by 11 weeks, characterized by erythema, hair loss, and scaling, resembling human psoriasis. Histopathology showed epidermal hyperplasia and other psoriasis-like features. The disease was not caused by bacteria or fungi and resolved with dexamethasone. Mice on a (PL/J x C57BL/6J)F1 background did not develop the disease, suggesting that a few genes, in addition to CD18, influence susceptibility. This model could help identify genes involved in inflammatory skin disorders.
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