Interferon‐γ production by cord‐blood mononuclear cells is reduced in newborns with a family history of atopic disease and is independent from cord blood IgE‐levels

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Abstract
For newborn children both elevated serum IgE levels in the cord blood and a positive family history of atopic disease have been shown to be risk factors for the manifestation of atopic diseases. In adult patients with atopic dermatitis, in vitro interferon-γ (IFN-γ) production is reduced and a negative correlation with serum IgE levels has been shown. We have now raised the question if newborn infants at risk for the development of atopic disease have similar abnormalities of cytokine production at birth. In vitro production of interleukin 2, interleukin 6 and interferon-γ by peripheral blood mononuclear cells was measured in 53 newborns: 21 had cord blood IgE levels above 0. 9 kU/1, 21 had a positive family history, 7 had both elevated IgE and a positive family history; 18 newborns with no identitiable risk for atopic disease served as controls. Umbilical cord blood mononuclear cells were stimulated with PHA or monoclonal antibody OKT3. In vitro production of interleukin 2 and 6 was comparable in all groups. Compared to controls IFN-γ production of peripheral mononuclear cells (PBMC) from newborns with elevated cord blood IgE was not different, but PMBC from newborns with a familial risk showed a significant decrease in PHA induced IFN-γ production (p < 0.005, U-test). No correlation between umbilical cord blood IgE and diminished IFN-γ production was found in newborns with or without a positive family history. We conclude that immunoregulatory abnormalities in newborns of atopic families are detectable already at birth and are unrelated to cord blood IgE.

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