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Originally published online as doi:10.2353/ajpath.2010.090488 on December 11, 2009

Published online before print December 11, 2009
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(American Journal of Pathology. 2010;176:246-258.)
© 2010 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2010.090488

Antigen-Specific Induction of Osteopontin Contributes to the Chronification of Allergic Contact Dermatitis

Anne M. Seier*, Andreas C. Renkl*, Guido Schulz*, Tanja Uebele*, Anca Sindrilaru*, Sebastian Iben*, Lucy Liaw{dagger}, Shigeyuki Kon{ddagger}, Toshimitsu Uede{ddagger} and Johannes M. Weiss*

From the Department of Dermatology and Allergology,* University of Ulm, Ulm, Germany; the Center for Molecular Medicine,{dagger} Maine Medical Center Research Institute, Scarborough, Maine; and the Division of Molecular Immunology,{ddagger} Institute of Genetic Medicine, Hokkaido University, Sapporo, Japan

Allergic contact dermatitis is a T cell-mediated immune response, which in its relapsing chronic form is of high socioeconomic impact. The phosphoglycoprotein osteopontin (OPN) has chemotactic and Th1 cytokine functions and in various models is essential for robust T cell-mediated immunity. Here we demonstrate that OPN is abundantly expressed by both effector T cells and keratinocytes in allergic contact dermatitis lesions. T cells from nickel-allergic donors secrete high levels of OPN following antigen-specific stimulation. OPN may substitute for missing IFN-{gamma} secretion in T effector cells because low IFN-{gamma}-producing T cell clones secrete high levels of OPN, and OPN down-modulates their interleukin-4 expression. Furthermore, interferon-{gamma} from T effector cells augments OPN in allergic contact dermatitis by inducing OPN in keratinocytes, which in turn polarizes dendritic cells and attracts inflammatory cells. In the murine contact hypersensitivity (CHS) model for allergic contact dermatitis, OPN is strongly induced in antigen-specific proliferating T cells, and OPN null mice display a reduced chronic CHS inflammatory response due to a decreased influx of effector T cells. Importantly, because of its function for chronic allergic contact dermatitis, OPN may well be a therapeutic target, because anti-OPN antibody treatment in part suppresses established chronic CHS.


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