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首页> 外文期刊>Science Immunology >IL-17–dependent fibroblastic reticular cell training boosts tissue protective mucosal immunity through IL-10–producing B cells
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IL-17–dependent fibroblastic reticular cell training boosts tissue protective mucosal immunity through IL-10–producing B cells

机译：IL-17依赖性的成纤维细胞网细胞训练通过产生IL-10的B细胞增强组织保护性粘膜免疫

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Prior experience of pathogen-associated stimuli reduces morbidity and mortality to newly encountered infections through innate immune training, which can be enhanced by childhood vaccination. Fibroblastic reticular cells (FRCs) are stromal cells in lymphoid organs that support lymphocyte localization and survival and modulate adaptive immune responses. IL-17 signaling is important for FRC metabolism and proliferation during inflammatory responses. Here, we show that FRC-intrinsic IL-17 signaling wasrequired for protective antibody-mediated immunity to the gut bacterial pathogen Citrobacter rodentium. We asked whether prior activation of FRC through nonspecific inflammatory “training” of the gut would alter subsequent immune response to C. rodentium. Inflammatory training increased the number of activated FRC in mesenteric LN (MLN) and enhanced the antibody response to C. rodentium in an IL-17–dependent manner. FRC demonstrated cardinal features of innate immune training, including increased epigenetic markers of activation and increased metabolic response to infection. Enhanced responses were still evident 6 weeks after training. The kinetics of bacterial infection were not changed by inflammatory training, but colon inflammation was paradoxically reduced. Mechanistically, IL-10 production by activated B cells was required for colon protective effects of inflammatory training. Enhancing tissue protective B cell responses thus led to increased production of antibody and IL-10, allowing clearance of infection with reduced tissue inflammation. These data identify a new mode of immune training through FRC to modulate future adaptive responses and better preserve host health.
机译：与病原体相关的刺激的先前经验可通过先天免疫训练降低发病率和死亡率，从而降低了新遇到的感染，这可以通过儿童疫苗接种来增强。成纤维细胞网状细胞（FRC）是支持淋巴细胞定位和存活并调节适应性免疫反应的淋巴器官中的基质细胞。 IL-17信号传导对于FRC代谢和炎症反应过程中的增殖很重要。在这里，我们表明FRC内膜IL-17信号传导是用于对肠道细菌病原体柠檬杆菌啮齿动物的保护性抗体介导的免疫的。我们询问事先通过非特异性炎症的肠道“训练”对FRC的事先激活是否会改变随后对啮齿动物的免疫反应。炎症训练增加了肠系膜LN（MLN）激活的FRC的数量，并以IL-17依赖性方式增强了对啮齿动物念珠菌的抗体反应。 FRC展示了先天免疫训练的基本特征，包括增加激活的表观遗传标记和对感染的代谢反应增加。训练后6周，仍有明显的反应仍然显而易见。细菌感染的动力学不会因炎症训练而改变，但结肠炎症是矛盾的。从机械上讲，炎症训练的结肠保护作用需要激活的B细胞产生IL-10。因此，增强组织保护性B细胞反应导致抗体和IL-10的产生增加，从而使感染清除，并减少组织炎症。这些数据通过FRC确定了一种新的免疫训练模式，以调节未来的适应性反应并更好地保护宿主健康。

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