Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2001
IFN-gamma production in response to IL-18 or IL-12 stimulation by peripheral blood mononuclear cells of atopic patients.
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Shikano H, Kato Z, Kaneko H, Watanabe M, Inoue R, Kasahara K, Takemura M, Kondo N
Аннотация
BACKGROUND: Several studies have shown that interleukin (IL)-4 and interferon-gamma (IFN-gamma) are important for the regulation of immunoglobulin E (IgE) production and that IL-18 and IL-12 induce IFN-gamma.
OBJECTIVE: IFN-gamma production in response to IL-18 or IL-12 stimulation was investigated in peripheral blood mononuclear cells (PBMCs) of atopic patients with various levels of serum IgE.
METHODS: Cytokine production from PBMCs was measured following stimulation with a non-specific stimulator (phytohemagglutinin: PHA), IL-18 or IL-12 in 12 healthy controls and 26 atopic patients with various serum IgE levels.
RESULTS: IFN-gamma production by IL-18-stimulated PBMCs was positively correlated with IFN-gamma production by IL-12-stimulated PBMCs (P < 0.05). However some atopic patients showed discrepancy between the levels of IFN-gamma production stimulated by IL-12 and by IL-18.
CONCLUSIONS: The results shown here suggest the presence of abnormalities in the IL-12 and/or IL-18 signalling pathways, such as genetic defects in the atopic patients.
OBJECTIVE: IFN-gamma production in response to IL-18 or IL-12 stimulation was investigated in peripheral blood mononuclear cells (PBMCs) of atopic patients with various levels of serum IgE.
METHODS: Cytokine production from PBMCs was measured following stimulation with a non-specific stimulator (phytohemagglutinin: PHA), IL-18 or IL-12 in 12 healthy controls and 26 atopic patients with various serum IgE levels.
RESULTS: IFN-gamma production by IL-18-stimulated PBMCs was positively correlated with IFN-gamma production by IL-12-stimulated PBMCs (P < 0.05). However some atopic patients showed discrepancy between the levels of IFN-gamma production stimulated by IL-12 and by IL-18.
CONCLUSIONS: The results shown here suggest the presence of abnormalities in the IL-12 and/or IL-18 signalling pathways, such as genetic defects in the atopic patients.