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首页> 外文期刊>Infection and immunity >Saturation of Immunoglobulin E (IgE) Binding Sites by Polyclonal IgE Does Not Explain the Protective Effect of Helminth Infections against Atopy
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Saturation of Immunoglobulin E (IgE) Binding Sites by Polyclonal IgE Does Not Explain the Protective Effect of Helminth Infections against Atopy

机译：免疫球蛋白E（IgE）结合位点的饱和多克隆IgE不能解释蠕虫感染对特应性的保护作用。

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One hypothesis for the decreased rates of atopy observed among helminth-infected individuals is that parasite-induced polyclonal immunoglobulin E (IgE) outcompetes allergen-specific IgE for FcεRI binding on basophils and mast cells. In experiments with fresh blood drawn from filaria-infected patients, we found no association between ratios of polyclonal to Brugia malayi antigen (BmAg)-specific IgE (range, 14:1 to 388:1) and basophil responses to BmAg as measured by histamine release. Using serum samples from a filaria-infected patient who also had dust mite (Dermatophagoides pteronyssinus)-specific IgE antibodies from time points with various ratios of polyclonal to D. pteronyssinus-specific IgE (16:1 to 86:1), we demonstrated that increased ratios of polyclonal to D. pteronyssinus-specific IgE did not attenuate basophil sensitization as measured by D. pteronyssinus-specific histamine release. Suppression of histamine release was likely not observed in either of these sets of experiments because polyclonal to antigen-specific IgE ratios were not sufficiently high, as concurrent passive sensitization of basophil experiments required ratios of polyclonal to antigen-specific IgE of greater than 500:1 to suppress basophil histamine release. Further, the intensity of IgE staining in basophil populations from 20 patients with active filaria infections correlated strongly with total serum IgE levels (rho = 0.698; P = 0.0024) with no plateau in intensity of IgE staining, even though some patients had total IgE levels of greater than 10,000 ng/ml. Our data therefore suggest that in helminth infections (and in filarial infections in particular), the ratios of polyclonal to allergen-specific IgE rarely reach those levels necessary to inhibit allergen-specific IgE-FcεRI binding and to suppress allergen-induced degranulation of mast cells and basophils.
机译：关于在蠕虫感染的个体中观察到的特异率降低的一种假设是，寄生虫诱导的多克隆免疫球蛋白E（IgE）胜过变应原特异性IgE的嗜碱性粒细胞和肥大细胞上FcεRI结合。在从感染丝虫病的患者中抽取新鲜血液进行的实验中，我们发现多克隆抗体与马来红血球抗原（BmAg）特异性IgE（范围为14：1至388：1）和嗜碱性粒细胞之间的比例没有关联通过组胺释放对BmAg的反应。使用来自丝虫感染患者的血清样本，这些患者在不同时间点都具有尘螨（ Dermatophagoides pteronyssinus ）特异的IgE抗体，且其多克隆与 D的比率不同。蕨类植物特异性的IgE（16：1至86：1），证明了多克隆抗体与 D的比例增加。翼状>肉特异性的IgE不能减弱嗜碱性粒细胞的致敏性，这是通过 D测定的。蕨类植物特异性组胺的释放。在这两组实验中均未观察到组胺释放的抑制，因为多克隆对抗原特异性IgE的比例不够高，因为嗜碱粒细胞实验的同时被动致敏要求多克隆对抗原特异性IgE的比例大于500：1。抑制嗜碱性粒细胞组胺的释放。此外，来自活跃丝虫感染的20例患者的嗜碱性粒细胞群体的IgE染色强度与总血清IgE水平密切相关（rho = 0.698; P = 0.0024），甚至没有IgE染色强度的平稳期尽管有些患者的总IgE水平大于10,000 ng / ml。因此，我们的数据表明，在蠕虫感染（尤其是丝虫感染）中，多克隆抗体与过敏原特异性IgE的比率很少达到抑制过敏原特异性IgE-FcεRI结合并抑制过敏原诱导的肥大细胞脱颗粒所必需的水平和嗜碱性粒细胞。

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