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Deficient interferon‐γ receptor‐mediated signaling in neonatal macrophages
Author(s) -
Maródi L
Publication year - 2002
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.2002.tb02915.x
Subject(s) - medicine , signal transduction , receptor , interferon , microbiology and biotechnology , immunology , biology
Aim : To describe functional and molecular characteristics of interferon‐γ (IFN‐γ) activation in neonatal mononuclear phagocytes (monocytes and macrophages). Methods and Results : Exposure of cord and adult macrophages to IFN‐γ gave quantitatively different results in Candida killing, as well as in release of superoxide anion (O 2 − ). At concentrations of 100 U ml −1 IFN‐γ, maximal increase in these functions with adult macrophages was achieved, whereas no enhancement of killing and O 2 − release by cord macrophages could be detected. Expression of IFN‐γ receptors was comparable on cord and adult cells and specific binding of [ 125 I]IFN‐γ to cord monocytes and macrophages was even higher compared with adult cells. By flow cytometry, elements of IFN‐γ receptor‐mediated signaling in cord and adult monocytes and macrophages were studied. Monoclonal antibodies against the native form of the signal transducer and activator of transcription‐1 (STAT‐1) revealed comparable expression of this protein in cord and adult macrophages. However, STAT‐1 phosphorylation in response to IFN‐γ was significantly decreased in neonatal monocytes ( p < 0.05) and macrophages ( p < 0.01) compared with adult cells. Conclusion : These data suggest deficient cytokine receptor signaling in neonatal mononuclear phagocytes exposed to IFN‐γ.