Preferential expression of T-cell receptor V beta-chains in atopic eczema.
Chronic skin colonization with Staphylococcus aureus is a characteristic feature of atopic eczema, and about 60% of S. aureus strains isolated from the skin of patients with atopic eczema secrete enterotoxins. T-cell stimulation by staphylococcal enterotoxins is restricted to the V beta-chain of the T-cell receptor. Therefore, the expression of different V beta-chains (V beta 3, 5 a,b,c, 6, 8, 12) on peripheral blood T-cells (CD4+) from patients with atopic eczema was measured by flowcytometry before and after stimulation with staphylococcal enterotoxin B. Lymphocytes from healthy donors served as controls. Additionally, the expression of V beta-chains in normal skin and in lesional skin of patients with atopic eczema was determined by immunofluorescence histology. In atopic eczema, higher numbers of CD4+ T-cells expressed V beta 3, V beta 8 and V beta 12 compared to the control group. No correlation between S. aureus enterotoxin B-stimulated V beta-expression and HLA-haplotypes was found. In lesional skin of patients with atopic eczema most of the infiltrating T-cells were V beta 3+, whereas in normal skin only very few T-cell receptor-expressing cells were detected. To evaluate the significance of these T-cell clones for allergic inflammation, T-cells from patients with atopic eczema and normal donors were stimulated with monoclonal antibodies against V beta 3, 5(c) and 8. Afterwards, the proliferative response of lymphocytes as well as IL-5 and IFN gamma synthesis were measured. T-cells from patients with atopic eczema showed a significantly higher proliferation and IL-5 secretion than normal donors after stimulation with monoclonal antibodies against V beta 3 and V beta 8. In contrast, the monoclonal antibodies directed to V beta 5(c) induced a markedly elevated proliferation and IFN gamma production of normal lymphocytes compared to patients with atopic eczema. Our results suggest a preferential expression of certain V beta-subgroups during inflammation in atopic eczema; this may be explained by a selective stimulation of TH2-cells via S. aureus-derived enterotoxins.
Neuber
K
K
Department of Dermatology, University Hospital Hamburg-Eppendorf, Germany.
Löliger
C
C
Köhler
I
I
Ring
J
J
D002478:Cells, Cultured; D003876:Dermatitis, Atopic / Q000276:immunology*; D004768:Enterotoxins / Q000494:pharmacology; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D006801:Humans; D007135:Immunoglobulin Variable Region / Q000032:analysis*; D007371:Interferon-gamma / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D008213:Lymphocyte Activation; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000032:analysis*; D012867:Skin / Q000276:immunology*; D013211:Staphylococcus aureus; D016176:T-Lymphocyte Subsets
D004768:Enterotoxins; D000949:Histocompatibility Antigens Class II; D007135:Immunoglobulin Variable Region; D015848:Interleukin-5; D016693:Receptors, Antigen, T-Cell, alpha-beta; C031818:enterotoxin B, staphylococcal; D007371:Interferon-gamma