Saturation of immunoglobulin E (IgE) binding sites by polyclonal IgE does not explain the protective effect of helminth infections against atopy
Saturation of immunoglobulin E (IgE) binding sites by polyclonal IgE does not explain the protective effect of helminth infections against atopy
复制标题
DOI：
10.1128/iai.73.7.4106-4111.2005
复制
发表时间：
2005-07-01
影响因子：
3.1
通讯作者：
Nutman, TB
中科院分区：
文献类型：
--
作者：
Mitre, E;Norwood, S;Nutman, TB
在蠕虫感染的个体中观察到的特应性比率降低的一个假设是，寄生虫诱导的多克隆免疫球蛋白E（IgE）在与嗜碱性粒细胞和肥大细胞结合的Fc ε RI方面胜过变应原特异性IgE。在实验中，从丝虫感染的患者抽取新鲜血液，我们没有发现多克隆马来丝虫抗原（BmAg）特异性IgE（范围，14：1至388：1）和嗜碱性粒细胞对BmAg的反应之间的关系，通过组胺释放测量。使用来自丝虫感染患者的血清样本，该患者同时具有尘螨（屋尘螨）特异性IgE抗体，其多克隆与屋尘螨特异性IgE的比例不同（16：1至86：1），我们证明了多克隆与屋尘螨特异性IgE的比例增加。用D.特异性组胺释放。在这两组实验中可能都没有观察到组胺释放的抑制，因为多克隆与抗原特异性IgE的比率不够高，因为嗜碱性粒细胞实验的同时被动致敏要求多克隆与抗原特异性IgE的比率大于500：1以抑制嗜碱性粒细胞组胺释放。此外，20例活动性丝虫感染患者的嗜碱性粒细胞群中IgE染色强度与血清总IgE水平密切相关（rho = 0.698; P = 0.0024），IgE染色强度无平台期，即使一些患者的总IgE水平大于10，000 ng/ml。因此，我们的数据表明，在蠕虫感染（特别是在丝虫感染）中，多克隆与过敏原特异性IgE的比例很少达到抑制过敏原特异性IgE-Fc β RI结合和抑制过敏原诱导的肥大细胞和嗜碱性粒细胞脱粒所必需的水平。
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 Fc epsilon RI 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-Fc epsilon RI binding and to suppress allergen-induced degranulation of mast cells and basophils.