Helminth infection protects mice from anaphylaxis via IL-10-producing B cells
Helminth infection protects mice from anaphylaxis via IL-10-producing B cells
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DOI：
10.4049/jimmunol.173.10.6346
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发表时间：
2004-11-15
影响因子：
4.4
通讯作者：
Fallon, PG
中科院分区：
文献类型：
--
作者：
Mangan, NE;Fallon, RE;Fallon, PG
感染者的过敏反应。在这项研究中，我们调查了实验感染曼氏血吸虫是否可以改变小鼠对极端过敏反应，过敏反应的易感性。我们正式证明了S.曼氏感染保护小鼠免于系统致命过敏反应的实验模型。研究表明，感染的蠕虫阶段可以介导这种保护作用。体内耗竭研究表明，B细胞和IL-10在蠕虫介导的保护中具有重要作用。此外，与未感染的小鼠相比，蠕虫感染的小鼠产生IL-10的B细胞的频率增加。然而，从蠕虫感染的小鼠或体外蠕虫调制的B细胞转移到致敏受体的B细胞加剧了过敏反应，这归因于IL-4产生的B细胞水平升高。蠕虫调制，IL-10产生B细胞从IL-4缺陷，但不是IL-5，IL-9或IL-13缺陷，小鼠转移到幼稚时，赋予完全抵抗过敏反应。因此，我们剖析了一种新的免疫调节机制，S。依赖于产生IL-10的B细胞群的曼氏蠕虫，其可以防止过敏性超敏反应。这些数据支持蠕虫免疫调节在卫生假说中的作用，并进一步说明寄生虫诱导的保护性调节（IL-10）反应和有害（IL-4）过敏反应之间的微妙平衡。
of allergic responses in infected individuals. In this study we investigated whether experimental infection with Schistosoma mansoni could alter the susceptibility of mice to an extreme allergic response, anaphylaxis. We formally demonstrate that S. mansoni infection protects mice from an experimental model of systemic fatal anaphylaxis. The worm stage of infection is shown to mediate this protective effect. In vivo depletion studies demonstrated an imperative role for B cells and IL-10 in worm-mediated protection. Furthermore, worm infection of mice increases the frequency of IL-10-producing B cells compared with that in uninfected mice. However, transfer of B cells from worm-infected mice or in vitro worm-modulated B cells to sensitized recipients exacerbated anaphylaxis, which was attributed to the presence of elevated levels of IL-4-producing B cells. Worm-modulated, IL-10-producing B cells from IL-4-deficient, but not IL-5-, IL-9- or IL-13-deficient, mice conferred complete resistance to anaphylaxis when transferred to naive.mice. Therefore, we have dissected a novel immunomodulatory mechanism induced by S. mansoni worms that is dependent on an IL-10-producing B cell population that can protect against allergic hypersensitivity. These data support a role for helminth immune modulation in the hygiene hypothesis and further illustrate the delicate balance between parasite induction of protective regulatory (IL-10) responses and detrimental (IL-4) allergic responses.