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首页> 外文期刊>Infection and immunity >Modulation of Human Immune Response by Echinococcus granulosus Antigen B and Its Possible Role in Evading Host Defenses
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Modulation of Human Immune Response by Echinococcus granulosus Antigen B and Its Possible Role in Evading Host Defenses

机译：细粒棘球E抗原B对人体免疫应答的调节及其在规避宿主防御中的可能作用

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By directly suppressing the function of certain immune cell subsets and by stimulating other cell populations related to immunopathology, parasite-derived substances play an important role in the chronic establishment of parasitic disease. Our objective was twofold: (i) to investigate further the role of Echinococcus granulosusantigen B (AgB) in the human early inflammatory response by determining its effect on polymorphonuclear cell (PMN) random migration, chemotaxis, and oxidative metabolism and (ii) to determine its action in acquired immunity by evaluating AgB and sheep hydatid fluid (SHF)-driven Th1 (gamma interferon [IFN-γ] and interleukin 12 [IL-12]) and Th2 (IL-4 and IL-13) cytokine production by peripheral blood mononuclear cells (PBMC) from 40 patients who had cured or stable or progressive cystic echinococcosis. AgB significantly inhibited PMN recruitment but left their random migration and oxidative metabolism unchanged. Patients' PBMC stimulated with AgB produced IL-4 and IL-13 but did not produce IL-12. They also produced significantly lower IFN-γ concentrations than did PBMC stimulated with SHF (P = 10?5). AgB skewed the Th1/Th2 cytokine ratios towards a preferentially immunopathology-associated Th2 polarization, predominantly in patients with progressive disease. AgB-stimulated patients' PBMC also proliferated less than SHF-stimulated PBMC (P = 9 × 10?3). In vitro Th2 cytokine production was reflected in vivo by elevated specific immunoglobulin E (IgE) and IgG4 antibodies binding to AgB. These findings confirm that AgB plays a role in the escape from early immunity by inhibiting PMN chemotaxis. They also add new information on the host-parasite relationship, suggesting that AgB exploits the activation of T helper cells by eliciting a nonprotective Th2 cell response.
机译：通过直接抑制某些免疫细胞亚群的功能并刺激其他与免疫病理学有关的细胞群，寄生虫衍生的物质在慢性寄生虫病的建立中起着重要的作用。我们的目标是双重的：（i）通过确定其对多形核细胞（PMN）随机迁移，趋化性的影响，进一步研究 Echinococcus granulosus 抗原B（AgB）在人类早期炎症反应中的作用。氧化代谢和（ii）通过评估AgB和绵羊羊水（SHF）驱动的Th1（γ干扰素[IFN-γ]和白介素12 [IL-12]）和Th2（IL-4和IL-13）来自40名已治愈或稳定或进行性囊性棘球co虫病患者的外周血单核细胞（PBMC）的细胞因子产生。 AgB显着抑制PMN募集，但其随机迁移和氧化代谢保持不变。用AgB刺激的患者PBMC产生IL-4和IL-13，但不产生IL-12。与SHF刺激的PBMC相比，它们产生的IFN-γ浓度也显着降低（ P = 10 ？5 ）。 AgB使Th1 / Th2细胞因子比率偏向于与免疫病理相关的Th2极化，主要发生于进行性疾病患者。 AgB刺激的患者PBMC的增殖也少于SHF刺激的PBMC（ P = 9×10 ？3 ）。体外Th2细胞因子的产生在体内通过提高的特异性免疫球蛋白E（IgE）和与AgB结合的IgG4抗体反映出来。这些发现证实，AgB通过抑制PMN趋化性在逃避早期免疫中发挥作用。他们还添加了有关宿主-寄生虫关系的新信息，表明AgB通过引发非保护性Th2细胞应答来利用T辅助细胞的激活。

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