De. Campbell et al., Intracellular interferon-gamma (IFN- gamma) production in normal children and children with atopic dermatitis, CLIN EXP IM, 115(3), 1999, pp. 377-382
A reduction in the in vitro production of IFN-gamma has been consistently d
escribed in atopic dermatitis (AD). Whether this reduction is due to a decr
ease in the population of peripheral blood mononuclear cells (PBMC) produci
ng 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-gam
ma in children with AD and in healthy non-atopic controls. As Staphylococcu
s aureus colonization is a feature of childhood AD, and is postulated to co
ntribute to the cutaneous inflammation in atopic dermatitis, S. aureus and
Staphylococcal enterotoxin B (SEB) were used to activate PBMC. Stimulated P
BMC from subjects with AD had significantly fewer IFN-gamma-containing cell
s in response to SEB (P < 0.001) and S. aureus (P < 0.01) than normal non-a
topic children. In addition, SEB-stimulated PBMC from children with AD had
less IFN-gamma per cell than normal non-atopic children (P < 0.01). Reducti
on 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 finding
s 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 re
duced amount of IFN-gamma production per cell. Furthermore, we found that t
his defect was not confined to CD4(+) T cells, suggesting a more generalize
d defect in IFN-gamma production in childhood AD.