Intracellular interferon-gamma (IFN-gamma) production in normal children and children with atopic dermatitis.

A reduction in the in vitro production of IFN-gamma has been consistently described in atopic dermatitis (AD). Whether this reduction is due to a decrease in the population of peripheral blood mononuclear cells (PBMC) producing IFN-gamma or reduced IFN-gamma production per cell, or a combination of both is not clear. We have examined the intracellular production of IFN-gamma in children with AD and in healthy non-atopic controls. As Staphylococcus aureus colonization is a feature of childhood AD, and is postulated to contribute to the cutaneous inflammation in atopic dermatitis, S. aureus and Staphylococcal enterotoxin B (SEB) were used to activate PBMC. Stimulated PBMC from subjects with AD had significantly fewer IFN-gamma-containing cells in response to SEB (P < 0.001) and S. aureus (P < 0.01) than normal non-atopic children. In addition, SEB-stimulated PBMC from children with AD had less IFN-gamma per cell than normal non-atopic children (P < 0.01). Reduction in the proportion of cells containing IFN-gamma was seen in CD4+, CD8+ and natural killer (NK) cells in PBMC from children with AD. Our findings indicate that reduced production of IFN-gamma observed in childhood AD is due to both a decrease in the number of IFN-gamma-producing cells and a reduced amount of IFN-gamma production per cell. Furthermore, we found that this defect was not confined to CD4+ T cells, suggesting a more generalized defect in IFN-gamma production in childhood AD.