Adhesion molecules in atopic dermatitis: patch tests elicited by house dust mite.
Different T-helper subsets, which are characterized by the secretion of distinct cytokines (Th1, Th2), have been found in house dust mite-exposed skin of sensitized individuals and in nickel-specific T lymphocytes from nickel contact allergic and non-allergic individuals. In order to evaluate the role which adhesion molecules may play in the homing of different T-cell subsets into allergen-exposed skin of atopic and normal individuals, we compared the expression pattern of adhesion molecules in patch test reactions to house dust mite antigen (D.pt.), nickel sulfate (Ni) and the irritant anthralin. Biopsies were taken at various time points after application of these agents and studied by immuncytochemistry. To exclude an endogenous difference in adhesion molecule expression in atopic and non-atopic skin, sequential biopsies from Ni patch tests of 2 normal individuals were also included in this study. The expression of E-selectin, P-selectin, CD31, VCAM-1 and ICAM-1 on endothelial cells and other cells in the skin was quantified by microscopic evaluation. Skin homing T cells were also quantified using antibodies to CD3, CD4, CD8, UCHL-1, L-selectin and the cutaneous lymphocyte antigen (CLA). Independent of the eliciting substance, all lesions showed an upregulation of all adhesion molecules tested, with the exception of CD62. The appearance of E-selectin and an increase in ICAM-1 and VCAM-1 expression were first observed at 12 h after application of the various agents. In parallel, the number of CLA+ and L-selectin+ lymphocytes increased steadily. No principle differences could be established between the various types of skin reactions in atopic individuals, nor did the skin of patients with AD differ from normal controls. Our results provide evidence that differential expression of adhesion molecules does not play a major part in observed differential homing of Th1 and Th2-cell subsets into patch test sites provoked by house dust mite and nickel sulfate in atopic and non-atopic individuals.
Jung
K
K
Clinic of Dermatology, Erfurt, Germany.
Linse
F
F
Pals
S T
ST
Heller
R
R
Moths
C
C
Neumann
C
C
D000818:Animals; D000875:Anthralin / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000032:analysis*; D003876:Dermatitis, Atopic / Q000276:immunology*; D004391:Dust; D019040:E-Selectin / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008925:Mites / Q000276:immunology*; D009532:Nickel / Q000276:immunology; D019007:P-Selectin / Q000032:analysis; D010328:Patch Tests; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D012867:Skin / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
D015815:Cell Adhesion Molecules; D004391:Dust; D019040:E-Selectin; D019007:P-Selectin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D009532:Nickel; D000875:Anthralin