Background The increased susceptibility of patients with atopic dermatitis (AD) to disseminated viral skin infections such as eczema herpeticum (ADEH+) is poorly understood. Objectives The primary goal of the current study was to determine whether ADEH+ subjects have identifiable defects in cell-mediated immunity that reduce their ability to control viral infections. Materials and methods In this study, we evaluated cytokine expression by various subsets of peripheral blood mononuclear cells from ADEH+ (n = 24) compared with AD without a history of viral infections (ADEH-) (n = 20) before and after treatment with herpes simplex virus (HSV). Results We found that interferon (IFN)-γ expression after HSV treatment was lower in the CD8+ T cells and monocytes from patients with ADEH+ compared with patients who are ADEH- or nonatopic. Given the induction of CD8+ T cells as the result of antigen presentation by human leucocyte antigen (HLA) class I, consistent with the findings described above we also found that the HLA B7 allele was significantly associated with risk of the ADEH+ phenotype (odds ratio = 1·91, P = 0·02, 125 ADEH+ and 161 ADEH- subjects). Conclusions These data suggest that defects in viral-induced IFN-γ from CD8+ T cells contribute to the ADEH+ phenotype. What's already known about this topic? Interferon (IFN)-γ-producing cells are known to be important cytotoxic effectors of immune protection against viruses. There have been limited reports of human leucocyte antigen (HLA) associations with risk of atopic dermatitis (AD), but there have been no reports of associations with risk of AD with eczema herpeticum (ADEH+). What does this study add? This study presents evidence that low IFN-γ expression in the CD8+ T-cell subset is associated with increased susceptibility of a subset of patients with AD to develop severe viral infections. The association of B7 alleles with EH in AD is significant because HLA B7 is more efficiently induced by IFN-γ than are HLA A locus products.
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