Feline atopic dermatitis: A model for Langerhans cell participation in disease pathogenesis

Petra J. Roosje, Diana Whitaker-Menezes, Michael H. Goldschmidt, Peter F Moore, Ton Willemse, George F. Murphy

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

Atopic dermatitis is a disorder characterized by cutaneous exanthemata as a consequence of exaggerated eczematous reactions to topical and systemic allergens. Langerhans cells, expressing CD1a and HLA-DR, and dermal dendritic cells, expressing HLA-DR, are known to be potent antigen-presenting cells and are thought to play an important role in the pathogenesis of atopic dermatitis. The immunophenotype of lesional skin in atopic dermatitis in humans involves increased numbers of CD1a+/MHC class II+ dendritic cells in addition to activated T cells, mast cells, and macrophages. To establish feline skin as a model for the study of human atopic dermatitis, and to elucidate the role of dendritic cells in feline atopic dermatitis, we investigated the presence of CD1a+ cells and MHC class II+ cells in the epidermis and dermis of lesional feline skin and in skin of healthy control animals. Immunohistochemistry revealed that MHC class II+ epidermal dendritic cells were CD1a+ in normal feline skin and significantly increased numbers of CD1a+ cells and MHC class II+ cells were present in the epidermis and dermis of lesional skin. These data provide the first correlative documentation of CD1a expression by feline dendritic cells containing Birbeck granules, and indicate the utility of feline skin in the study of human cutaneous atopy.

Original languageEnglish (US)
Pages (from-to)927-932
Number of pages6
JournalAmerican Journal of Pathology
Volume151
Issue number4
StatePublished - Oct 1997

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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    Roosje, P. J., Whitaker-Menezes, D., Goldschmidt, M. H., Moore, P. F., Willemse, T., & Murphy, G. F. (1997). Feline atopic dermatitis: A model for Langerhans cell participation in disease pathogenesis. American Journal of Pathology, 151(4), 927-932.