Preferential expression of T-cell receptor Vβ-chains in atopic eczema

Abstract

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 Vβ-chain of the T-cell receptor. Therefore, the expression of different Vβ-chains (Vβ3, 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 Vβ-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 Vβ3, Vβ8 and Vβ12 compared to the control group. No correlation between S. aureus enterotoxin B-stimulated Vβ-expression and HLA-haplotypes was found. In lesional skin of patients with atopic eczema most of the infiltrating T-cells were Vβ3+, 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 Vβ3, 5(c) and 8. Afterwards, the proliferative response of lymphocytes as well as IL-5 and IFNγ 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 Vβ3 and Vβ8. In contrast, the monoclonal antibodies directed to Vβ5(c) induced a markedly elevated proliferation and IFNγ production of normal lymphocytes compared to patients with atopic eczema. Our results suggest a preferential expression of certain Vβ-subgroups during inflammation in atopic eczema; this may be explained by a selective stimulation of T(H)2-cells via S. aureus-derived enterotoxins.