Klouche M, Klinger M H, Kühnel W, Wilhelm D
Institute of Immunology and Transfusion Medicine, University of LübeckMedical School, Germany.
J Allergy Clin Immunol. 1997 Aug;100(2):235-41. doi: 10.1016/s0091-6749(97)70230-6.
Platelets of atopic individuals differ in alpha-granular contents and in the amount of biologically active mediators released compared with platelets of nonatopic subjects. Because platelets carry the low-affinity IgE receptor (CD23), they may contribute to long-lasting IgE sensitivity by serving as a storage pool for IgE. We compared 45 atopic individuals with immediate-type allergies and 25 nonatopic control subjects with respect to storage and release of IgE by their platelets. Platelets of atopic individuals were characterized by a 10-fold higher median IgE content compared with those of nonatopic control subjects. The platelet IgE content correlated with the serum IgE level in the four atopic individuals with seasonal allergies who were followed up monthly over 1 year. Platelet stimulation with platelet activating factor, but not with thrombin or adenosine diphosphate, resulted in a release of 65% of the stored IgE. Conversely, platelet stimulation with monoclonal IgE/kappa resulted in the release of the chemokine RANTES. Platelet alpha-granules were identified as the main storage compartment for IgE by postembedding immunocytochemistry. Although more than half of the alpha-granules showed gold labeling for IgE, additional labeling was found on the external face of the plasma membrane and within the open canalicular system, indicating endocytosis and exocytosis of IgE. Moreover, the detection of CD23 not only on the plasma membrane but also on membranes of the alpha-granules further supports the existence of an exchange of IgE between the blood plasma and an internal storage compartment. Endocytosis could be confirmed by the uptake of an IgE myeloma protein coupled to colloidal gold. We conclude that platelets of atopic individuals may contribute to allergic inflammation by serving as a storage pool for IgE and by their increased capacity to liberate further mediators of allergy in response to IgE stimulation.
与非特应性个体的血小板相比，特应性个体的血小板在α颗粒内容物以及释放的生物活性介质数量方面存在差异。由于血小板携带低亲和力IgE受体（CD23），它们可能通过作为IgE的储存库而有助于持久的IgE敏感性。我们比较了45名具有速发型过敏反应的特应性个体和25名非特应性对照个体血小板中IgE的储存和释放情况。特应性个体的血小板特征是，其IgE含量中位数比非特应性对照个体高10倍。在4名患有季节性过敏的特应性个体中，对其进行了为期1年的每月随访，结果显示血小板IgE含量与血清IgE水平相关。用血小板活化因子刺激血小板可导致65%储存的IgE释放，但用凝血酶或二磷酸腺苷刺激则不会。相反，用单克隆IgE/κ刺激血小板会导致趋化因子RANTES释放。通过包埋后免疫细胞化学鉴定血小板α颗粒是IgE的主要储存区室。虽然超过一半的α颗粒显示有IgE的金标记，但在质膜外表面和开放小管系统内也发现了额外的标记，表明存在IgE的内吞作用和外排作用。此外，不仅在质膜上而且在α颗粒膜上检测到CD23，这进一步支持了血浆与内部储存区室之间存在IgE交换。通过摄取与胶体金偶联的IgE骨髓瘤蛋白可证实内吞作用。我们得出结论，特应性个体的血小板可能通过作为IgE的储存库以及其在IgE刺激下释放更多过敏介质的能力增强，从而促进过敏性炎症。
