Paganelli R, Scala E, Capobianchi M R, Fanales-Belasio E, D'Offizi G, Fiorilli M, Aiuti F
Department of Allergy and Clinical Immunology, University La Sapienza, Rome, Italy.
Clin Exp Immunol. 1991 Apr;84(1):28-33.
We measured the in vitro production of interferon-gamma (IFN-gamma) in five cases of hyper-IgE syndrome (HIgE), induced by mitogens, calcium ionophores and phorbol ester. The biosynthesis of IFN-gamma was severely reduced or undetectable in HIgE, while it was near normal in most atopic patients. The in vitro spontaneous production of IgE was increased overall in HIgE patients, although no correlation was found with serum IgE levels. Recombinant interleukin-4 (IL-4) induced a further increase in IgE synthesis, and its effect was totally antagonized by recombinant IFN-gamma; the same pattern of response was also observed in atopic subjects with high production of IgE. IFN-alpha synergized with IL-4 on IgE synthesis, whereas recombinant IL-6 gave opposite changes in individual cases tested. We propose that IFN-gamma deficiency may be responsible for some of the features of HIgE patients, including IgE levels and infections.
我们检测了5例高免疫球蛋白E综合征(HIgE)患者在有丝分裂原、钙离子载体和佛波酯诱导下的γ干扰素(IFN-γ)体外产生情况。在HIgE患者中,IFN-γ的生物合成严重减少或无法检测到,而在大多数特应性患者中其水平接近正常。虽然未发现与血清IgE水平相关,但HIgE患者的IgE体外自发产生总体上有所增加。重组白细胞介素-4(IL-4)可诱导IgE合成进一步增加,其作用完全被重组IFN-γ拮抗;在高IgE产生的特应性受试者中也观察到相同的反应模式。IFN-α与IL-4协同促进IgE合成,而重组IL-6在个别测试病例中产生相反的变化。我们认为,IFN-γ缺乏可能是导致HIgE患者某些特征的原因,包括IgE水平和感染。