Lichtenstein L M
J Immunol. 1975 Jun;114(6):1692-9.
The mechasism of human basophil histamine release by the calcium ionophore A23187 has been compared to that induced by the interaction of antigen with cell bound IgE antibody. Ionophore induced histamine release (Ion. H.R.) occurs with the leukocytes of both normal and allergic donors. It is completely calcium dependent; LaCl3 inhibits both Ion. H.R. and antigen induced histamine release (Ag. H.R.) at about 10-minus 7 M. The kinetics of Ion. H.R. suggest that this process has no "desensitization" phase as does Ag. H.R. and the ionophore is fully active on antigen-desensitized cells. Pharmacologic studies indicate that dibutyryl cyclic AMP and agents which increase endogenous cyclic AMP levels do not inhibit Ion. H.R. as they inhibit the early stages of Ag. H.R. Of the agents which affect microtubules, colchicine inhibits and D2O enhances Ion. H.R. in a manner which is qualitatively similar but quantitatively less marked than their effects on Ag. H.R. The metabolic antagonist 2-deoxyglucose inhibits both Ion. H.R. and Ag. H.R. in a similar fashion. Based on these data and the observation that cells pretreated with ionophore show a marked (synergistic) enhancement of Ag. H.R. we conclude that Ion. H.R. has a similar or identical mechanism to the later stages if Ag. H.R. but "short circuits" the cyclic AMP-associated events of Ag. H.R.
钙离子载体A23187诱导人嗜碱性粒细胞组胺释放的机制已与抗原与细胞结合的IgE抗体相互作用所诱导的机制进行了比较。离子载体诱导的组胺释放（Ion. H.R.）在正常供体和过敏供体的白细胞中均会发生。它完全依赖于钙；LaCl3在约10^-7 M时可抑制Ion. H.R.和抗原诱导的组胺释放（Ag. H.R.）。Ion. H.R.的动力学表明，该过程没有像Ag. H.R.那样的“脱敏”阶段，并且离子载体在抗原脱敏的细胞上具有完全活性。药理学研究表明，二丁酰环磷酸腺苷和增加内源性环磷酸腺苷水平的药物不会像抑制Ag. H.R.的早期阶段那样抑制Ion. H.R.。在影响微管的药物中，秋水仙碱抑制而重水增强Ion. H.R.，其方式在质量上相似，但在数量上比它们对Ag. H.R.的影响小。代谢拮抗剂2-脱氧葡萄糖以类似的方式抑制Ion. H.R.和Ag. H.R.。基于这些数据以及用离子载体预处理的细胞显示出Ag. H.R.显著（协同）增强的观察结果，我们得出结论，Ion. H.R.与Ag. H.R.后期阶段具有相似或相同的机制，但“绕过”了Ag. H.R.中与环磷酸腺苷相关的事件。
