Association of the proliferation of CD4(+)/Vbeta17(+) cells and peripheral blood mononuclear cells in response to staphylococcal enterotoxin B(SEB) in atopic dermatitis / 천식및알레르기

ABSTRACT

BACKGROUND AND OBJECTIVE: Atopic dermatitis(AD) is a chronic inflammatory skin disease with a high incidence in early childhood. Staphylococcus aureus(SA) is found at high concentrations in over 90% of AD skin lesions compared with 5-37% of age-matched controls. SA isolates from AD subjects have a high prevalence(37-57%) of superantigen-producing strains. And staphylococcal enterotoxin B(SEB) has been shown to induce inflammatory reactions following application to intact skin of normal and atopic subjects. These findings suggest that SA toxin produced by SA may be linked with initiation or aggravation of AD, but the role of satphylococcal enterotoxin to the T cell in the pathogenesis of AD has not been determined clearly. This study was conducted to determine whether staphylococcal enterotoxin might have a role as a superantigen in the pathogenesis of AD. Materials and Method: We investigated the proliferative responses of peripheral blood mononuclear cell(PBMC) from 8 patients with AD and 10 age-matched normal controls. We also assessed T cell markers and T cell receptor(TCR) Vbeta chain expression by flow cytometry with and without SEB stimulation. RESULTS: PBMC from AD patients showed increased proliferation to SEB 100 pg/ml and 1000 pg/ml compared to controls. There were no differences of CD3(+), CD4(+), and CD8(+) cells after SEB stimulation between the two groups. And there were also no differences of TCR Vbeta2(+) and TCR Vbeta8(+) cells with and without SEB stimulation, but TCR Vbeta17(+) cells were increased after SEB stimulation not only in AD patients but also in controls compared to culture without SEB. The expressions of TCR Vbeta17 chain of CD3(+) and CD4(+) cells after SEB stimulation were increased in AD patients compared to controls. Furthermore, there was positive correlation between the enhanced PBMC proliferative responses to SEB and increased expressions of SEB reactive TCR Vbeta17(+)/CD4(+) cells in AD patients and controls. CONCLUSION: These findings suggest that SEB is important in the pathogenesis of atopic dermatitis and also provide evidence that the increased use of certain TCR Vbeta families is of functional significance.