Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands.
Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, UK.
Eur J Immunol. 2019 Aug;49(8):1226-1234. doi: 10.1002/eji.201847858. Epub 2019 May 29.
The helminth Schistosoma mansoni (S. mansoni) induces a network of regulatory immune cells, including interleukin (IL)-10-producing regulatory B cells (Bregs). However, the signals required for the development and activation of Bregs are not well characterized. Recent reports suggest that helminths induce type I interferons (IFN-I), and that IFN-I drive the development of Bregs in humans. We therefore assessed the role of IFN-I in the induction of Bregs by S. mansoni. Mice chronically infected with S. mansoni or i.v. injected with S. mansoni soluble egg antigen (SEA) developed a systemic IFN-I signature. Recombinant IFN-α enhanced IL-10 production by Bregs stimulated with S. mansoni SEA in vitro, while not activating Bregs by itself. IFN-I signaling also supported ex vivo IL-10 production by SEA-primed Bregs but was dispensable for activation of S. mansoni egg-induced Bregs in vivo. These data indicate that although IFN-I can serve as a coactivator for Breg IL-10 production, they are unlikely to participate in the development of Bregs in response to S. mansoni eggs.
曼氏血吸虫（S. mansoni）诱导了一个调节性免疫细胞网络，包括产生白细胞介素（IL）-10 的调节性 B 细胞（Bregs）。然而，Bregs 发育和激活所需的信号尚未得到很好的描述。最近的报告表明，寄生虫诱导 I 型干扰素（IFN-I），而 IFN-I 驱动人类 Bregs 的发育。因此，我们评估了 IFN-I 在曼氏血吸虫诱导 Bregs 中的作用。慢性感染曼氏血吸虫或静脉注射曼氏血吸虫可溶性卵抗原（SEA）的小鼠会发展出全身 IFN-I 特征。重组 IFN-α增强了体外用 S. mansoni SEA 刺激的 Bregs 产生 IL-10，而自身不激活 Bregs。IFN-I 信号也支持 SEA 启动的 Bregs 的体外 IL-10 产生，但对体内 S. mansoni 卵诱导的 Bregs 的激活是可有可无的。这些数据表明，尽管 IFN-I 可以作为 Breg IL-10 产生的共激活剂，但它们不太可能参与对 S. mansoni 卵的 Bregs 发育的反应。
