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首页> 外文期刊>Infection and immunity >Interleukin-10 and Antigen-Presenting Cells Actively Suppress Th1 Cells in BALB/c Mice Infected with the Filarial Parasite Brugia pahangi
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Interleukin-10 and Antigen-Presenting Cells Actively Suppress Th1 Cells in BALB/c Mice Infected with the Filarial Parasite Brugia pahangi

机译：白细胞介素10和抗原呈递细胞积极抑制丝虫寄生性布鲁氏菌感染的BALB / c小鼠中的Th1细胞。

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Infection with the third-stage larvae (L3) of the filarial nematodeBrugia results in a Th2-biased immune response in mice and humans. Previously we have shown that the production of interleukin 4 (IL-4) is critical for down-regulating polyclonal Th1 responses in L3-infected mice. However, the in vitro neutralization of IL-4 did not fully recover the defective polyclonal Th1 responses, nor did it result in the production of any antigen (Ag)-specific Th1 cytokines, suggesting that perhaps infection with L3 does not result in priming of Th1 cells in vivo. In this study, we analyzed the role of IL-10 and Ag-presenting cells (APCs) in the spleen as additional factors controlling the Th2 bias in infected mice. Our data show that IL-10 and APCs also contribute to the suppression of mitogen-driven Th1 responses of spleen cells from infected mice. In addition, the neutralization of IL-10 or the replacement of the resident APC population from spleen cell cultures resulted in the production of Ag-specific Th1 cytokines. Irradiated spleen cells from either L3-infected or uninfected mice were able to restore Ag-specific Th1 responses in vitro. Therefore, it appears that Brugia-reactive Th1 cells are primed following infection with L3, but are actively suppressed in vivo by a mechanism that involves IL-10 and the resident APC population, but not IL-4. These results indicate that a complex interplay of cytokines and cell populations underscores the Th2-polarized response in L3-infected mice.
机译：感染丝状线虫 Brugia 的第三阶段幼虫（L3）会导致小鼠和人类的Th2偏向免疫反应。以前我们已经表明，白细胞介素4（IL-4）的产生对于下调感染L3的小鼠中的多克隆Th1反应至关重要。然而，IL-4的体外中和不能完全恢复有缺陷的多克隆Th1反应，也不会导致产生任何抗原（Ag）特异性Th1细胞因子，这表明L3感染可能不会导致L3的启动。体内Th1细胞。在这项研究中，我们分析了脾脏中IL-10和Ag呈递细胞（APC）作为控制感染小鼠Th2偏倚的其他因素的作用。我们的数据表明，IL-10和APCs也有助于抑制受感染小鼠脾细胞的有丝分裂原驱动的Th1反应。此外，IL-10的中和作用或脾细胞培养物中常驻APC种群的替代导致产生Ag特异性Th1细胞因子。来自L3感染或未感染小鼠的脾脏细胞能够在体外恢复Ag特异性Th1反应。因此，看来 Brugia 反应性Th1细胞在被L3感染后被启动，但在体内被IL-10和驻留的APC群体（而非IL-4）所抑制。这些结果表明，细胞因子和细胞群之间复杂的相互作用强调了感染L3的小鼠的Th2极化反应。

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