title: Loss of cutaneous delayed hypersensitivity reactions in nevus anemicus. Evidence for close concordance of cutaneous delayed hypersensitivity and endothelial E-selectin expression.
abstract: BACKGROUND
  The relationship of adhesion molecules in the dermis to immunologically mediated cutaneous inflammation can be understood by focusing on a serendipitous phenomenon: a lack of dermatitis within the margins of a nevus anemicus (NA) in generalized contact dermatitis. The expression and induction of endothelial and epithelial adhesion molecules with intradermally injected cytokines were investigated.
  
  
  METHODS
  Nevus anemicus without dermatitis lacked histopathological changes consistent with inflammatory cellular infiltration. The surrounding skin of the dermatitic lesion expressed HLA-DR, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1, and E-selectin on endothelial cells, and HLA-DR and ICAM-1 in the epidermis. However, the skin of the NA lacked endothelial E-selectin and epidermal HLA-DR and ICAM-1 expression. Interferon gamma, injected intradermally, induced endothelial and epidermal HLA-DR and ICAM-1 expression in the NA and surrounding normal skin. While interferon gamma strongly induced E-selectin expression on endothelial cells in normal skin, it failed to induce endothelial E-selectin expression in the NA.
  
  
  CONCLUSIONS
  This study suggests that vessels in the NA do not respond normally to proinflammatory cytokines, at least at the level of E-selectin expression. The absence of keratinocyte ICAM-1 and HLA-DR expression in the NA lesion in contact dermatitis is likely caused by the absence of infiltrating lymphocytes, rather than by the intrinsic unresponsiveness of keratinocytes to interferon gamma. Among the endothelial cell adhesion molecules in delayed hypersensitivity, E-selectin appears to be indispensable in recruiting circulating T lymphocytes to the skin.
authors.affiliation: Department of Dermatology, Faculty of Medicine, Mie University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Mizutani
authors.forename: S
authors.initials: S
authors.lastname: Ohyanagi
authors.forename: Y
authors.initials: Y
authors.lastname: Umeda
authors.forename: M
authors.initials: M
authors.lastname: Shimizu
authors.forename: T S
authors.initials: TS
authors.lastname: Kupper
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis; D017449:Dermatitis, Allergic Contact / Q000150:complications / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D019040:E-Selectin / Q000096:biosynthesis*; D004727:Endothelium / Q000378:metabolism; D005260:Female; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006222:Hamartoma / Q000150:complications / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis
chemical_list: D015703:Antigens, CD; D019040:E-Selectin; D006684:HLA-DR Antigens; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1