Circulating T cells from four patients with the hyper-IgE syndrome were found to produce significantly lower concentrations of interferon-gamma (IFN-γ) in response to stimulation with phytohemagglutinin (PHA) than did T cells from eight age-matched healthy controls, three patients with atopic dermatitis and one patient with chronic granulomatous disease. A clonal analysis revealed that patients with hyper-IgE syndrome had markedly lower proportions of circulating T cells able to produce IFN-γ and tumor necrosis factor-α (TNF-α) in comparison with controls. In contrast, the proportions of peripheral blood T cells able to produce IL-4 or IL-2 were not significantly different in patients and controls. All the four patients with hyper-IgE syndrome showed high proportions of circulating CD4+ helper T cells able to induce IgE synthesis in allogeneic B cells, as well. Such an activity for IgE synthesis appeared to be positively correlated with IL-4 production by T cells and inversely related to the ability of the same T cells to produce IFN-γ. Since IFN-γ exerts an inhibitory effect on the synthesis of IgE and both IFN-γ and TNF-α play an important role in inflammatory reactions, we suggest that the defective production of IFN-γ may be responsible for hyperproduction of IgE and the combined defect of IFN-γ and TNF-α may contribute to the undue susceptibility to infections seen in patients with hyper-IgE syndrome.
|Number of pages||6|
|Journal||Journal of Clinical Investigation|
|Publication status||Published - 1989|
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