Evidence that defective interferon-gamma production in dermatitis patients is due to intrinsic abnormalities

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Abstract
The in vitro production of interferon-gamma (IFN-.gamma.) in 19 atopic dermatitis (AD) patients was compared with that of 12 controls. IFN-.gamma. production by phytohaemagglutinin (PHA) stimulated peripheral blood mononuclear cells (PBMC) was profoundly diminished in AD patients, whereas the proliferative response was similar to that of control PBMC. The addition of 40 U/ml of interleukin-2 (IL-2) to the cultures failed to restore IFN-.gamma. production. Similarly, removal of adherent cells also had no effect. Reduced IFN-.gamma. secretion was observed after stimulation with the CD3 monoclonal antibody OKT3, ionomycin + 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or with high levels of IL-2 (200 U/ml). There were increased proportions of CD4+ T helper/inducer cells and decreased proportions of CD8+ T cytotoxic-/suppressor cells and CD16+ natural killer (NK) cells in AD patients. This resulted in an increased CD4/CD8 ratio as compared with controls, but no correlation was observed between numbers of T cell subpopulations and IFN-.gamma. generation. However, a significant correlation was found between IFN-.gamma. generation in vitro and IgE serum concentration in AD patients. The data suggest that the decreased production of IFN-.gamma. by AD patients is due to intrinsic differences in capacity to produce this cytokine and is not the result of differences in regulatory cell interactions. Moreover, the findings indicate that decreased production of IFN-.gamma. may be an important factor in the pathogenesis of this disease.

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