Geha R S, Leung D Y
Int Arch Allergy Appl Immunol. 1987;82(3-4):389-91. doi: 10.1159/000234234.
Over the last several years our laboratory has been engaged in the in vitro study of the regulation of IgE synthesis. We have found that polyclonal B cell activators fail to induce IgE synthesis in human B cells. Alloreactive T cell helper clones induced synthesis in B cells only under conditions of interaction and in B cells from allergic donors under cognate conditions of bystander stimulation as well. Isotype-specific regulation of the IgE response was mediated in the secretion of IgE-binding factors by T cells suppressing Fc receptors for IgE. Finally, IgE immune complexes in sera from patients with hyper-IgE states were shown to downregulate T cell proliferation to antigen and to stimulate monocytes to resorb 45Ca-labelled bone and to release prostaglandins. The implications of these in vitro findings for disease states in which IgE is elevated are discussed.
在过去几年里，我们实验室一直致力于IgE合成调节的体外研究。我们发现多克隆B细胞激活剂不能诱导人B细胞合成IgE。同种异体反应性T细胞辅助克隆仅在相互作用的条件下以及在旁观者刺激的同源条件下，才能诱导来自过敏供体的B细胞合成IgE。IgE反应的同种型特异性调节是由抑制IgE Fc受体的T细胞分泌IgE结合因子介导的。最后，高IgE状态患者血清中的IgE免疫复合物被证明可下调T细胞对抗原的增殖，并刺激单核细胞吸收45Ca标记的骨并释放前列腺素。本文讨论了这些体外研究结果对IgE升高的疾病状态的意义。
