Atopic eczema is thought to be caused by skin-infiltrating CD4 T cells
of the Th1-like and/or Th2-like subtype. We assessed expression of th
e Th1-like cytokine, interferon-gamma, and the Th2-like cytokine, inte
rleukin-4, in lesional atopic skin. Compared with that in normal skin,
interferon-gamma and interleukin-4 mRNA expression were increased in
eczematous skin lesions in 13 and 4 of 15 patients, respectively. Afte
r successful therapy of atopic dermatitis, the increased interferon-ga
mma mRNA expression but not the increased interleukin-4 mRNA expressio
n was significantly down-regulated. These data indicate that in-situ e
xpression of interferon-gamma is linked to the clinical course of atop
ic dermatitis.