
* Division of Dermatology, Sunnybrook and Womens College Health Science Centre, University of Toronto, Ontario, Canada M4N 3M5, and
Department of Dermatology, University "G.dAnnunzio", Via dei Vestini Chieti, Italy
Correspondence: Dr. Daniel N. Sauder, Professor and Chairman, Johns Hopkins University, Suite 1002, 550 N. Broadway, Baltimore, MD 21205. E-mail: dsauder{at}jhmi.edu
Contact hypersensitivity (CHS), a dendritic-cell (DC)-dependent, T-cell-mediated skin immune response to reactive haptens, has been a subject of intense research for many years. The molecular mechanisms underlying CHS are complicated and are not fully understood. During the past few years, varieties of gene-targeted knockout mice have been used in the study of CHS. Such studies have contributed significantly to our understanding of the mechanisms responsible for the initiation of CHS. This review focuses on insights into molecular requirements for CHS gained from knockout studies.
Key Words: dendritic cell hapten CHS mouse targeted mutation
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