Platelet augmentation of IgE-dependent histamine release from human basophils and mast cells.

Platelet augmentation of IgE-dependent histamine release from human basophils and mast cells.
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血小板增强人类嗜碱性粒细胞和肥大细胞中 IgE 依赖性组胺的释放。

DOI:
10.1159/000233511
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发表时间:
1984
期刊:
International archives of allergy and applied immunology
影响因子:
--
通讯作者:
Lichtenstein,LM
Lichtenstein,LM
中科院分区:
--
文献类型:
--
作者:
Knauer,KA;Kagey-Sobotka,A;AdkinsonJr,NF;Lichtenstein,LM

文献摘要

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人血小板中的一种因子可增强 IgE 介导的人嗜碱性粒细胞和肥大细胞释放组胺。这种作用与血小板数量直接相关;在生理血小板/白细胞比例 (40:1) 下,增强程度为 66 ± 11%。凝血酶对血小板的刺激作用增强了一倍以上,在 40:1 时达到 172 ± 10%。肥大细胞的释放也被血小板增强,尽管幅度更有限(与凝血酶的 40:1 时为 86 ± 13%)。不需要直接接触嗜碱性粒细胞/血小板,因为血小板上清液是完全活跃的;然而,血小板因子增强了相对于其他白细胞纯化 100 倍的嗜碱性粒细胞,这表明血小板因子/嗜碱性粒细胞存在直接相互作用。血小板增强活性的出现与α颗粒标记物(PF4)的释放有关,而不是与花生四烯酸代谢产物(血栓烷B2)有关。造成这些影响的血小板因子不可透析,具有热稳定性,并且与 PF4 或血小板衍生生长因子 (PDGF) 不同。由于抗 IgE 刺激的嗜碱性粒细胞导致 PF4 释放,并且这与增强因子的释放相关,因此我们认为存在促炎前馈关系。结合我们之前的数据显示血小板在过敏性哮喘受试者的抗原攻击期间在体内被激活,这些结果表明血小板可能在调节人类 IgE 介导的过敏反应中发挥重要作用。
A factor(s) from human platelets enhances IgE-mediated histamine release from human basophils and mast cells. This effect is directly related to the platelet number; at physiological platelet/leukocyte ratios (40:1), the enhancement was 66 ± 11 %. Platelet stimulation by thrombin more than doubled the enhancement, to 172 ± 10% at 40:1. Mast cell release was also enhanced by platelets although the magnitude was more limited (86 ± 13% at 40:1 with thrombin). Direct basophil/platelet contact was unnecessary in that platelet supernatants were fully active; a direct platelet factor/basophil interaction is suggested, however, by the fact that basophils purified 100-fold with respect to other leukocytes were enhanced by the platelet factors. The appearance of platelet-enhancing activity is associated with the release of an alpha-granule marker (PF4) rather than with products of arachidonic acid metabolism (thromboxane B2). The platelet factor(s) responsible for these effects are not dialyzable, are heat stable and do not appear to be identical to PF4or platelet-derived growth factor (PDGF). Since anti-IgE-stimulated basophils cause PF4release and this correlates with the release of enhancing factor, we suggest that a pro-inflammatory feed forward relationship exists. Together with our previous data showing that platelets are activated in vivo during antigen challenge of allergic asthmatic subjects, these results suggest that platelets may be important in modulating IgE-mediated allergic reactions in man.