Romagnani S, Del Prete G, Maggi E, Parronchi P, Tiri A, Macchia D, Giudizi M G, Almerigogna F, Ricci M
Allergology and Clinical Immunology, University of Florence, Firenze, Italy.
Clin Immunol Immunopathol. 1989 Jan;50(1 Pt 2):S13-23. doi: 10.1016/0090-1229(89)90110-4.
Studies of human IgE synthesis are summarized and provide further insight into the cellular and molecular mechanisms involved in IgE regulation, as well as in the alterations responsible for IgE disregulation in some pathological conditions. These include the demonstration that IL-4 is the essential factor for the induction of human IgE syntheses. Another T cell-derived lymphokine, IFN-gamma negatively regulated the IgE synthesis induced by IL-4. These two lymphokines can be produced by different T helper cells, as shown in mice, but they can also be the product of the same T cells clones. Additional cellular and/or molecular signals appear to be involved in the IL-4-induced IgE synthesis, but their precise role in this process is undetermined. Finally, alternations of one or more of these regulatory mechanisms can be detected in patients with pathological conditions characterized by hyperproduction of IgE. In particular, the increased prevalence of T cells clones able to produce IL-4 appears to be a distinctive feature of patients with common atopy whereas a reduction in the proportion of IFN-gamma-producing T cells seems to be peculiar of both patients with hyper-IgE syndrome and patients with AIDS.
对人类IgE合成的研究进行了总结，为深入了解IgE调节所涉及的细胞和分子机制，以及某些病理状况下导致IgE调节异常的改变提供了更多信息。这些研究包括证实白细胞介素-4（IL-4）是诱导人类IgE合成的关键因素。另一种T细胞衍生的淋巴因子，γ干扰素（IFN-γ）对IL-4诱导的IgE合成起负调节作用。如在小鼠中所示，这两种淋巴因子可由不同的辅助性T细胞产生，但它们也可能是同一T细胞克隆的产物。IL-4诱导的IgE合成似乎还涉及其他细胞和/或分子信号，但其在这一过程中的精确作用尚不确定。最后，在以IgE过度产生为特征的病理状况患者中，可检测到这些调节机制中的一种或多种发生改变。特别是，能够产生IL-4的T细胞克隆的患病率增加似乎是常见特应性患者的一个显著特征，而产生IFN-γ的T细胞比例降低似乎是高IgE综合征患者和艾滋病患者所特有的。
