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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Schistosoma mansoni triggers Dectin-2, which activates the Nlrp3 inflammasome and alters adaptive immune responses
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Schistosoma mansoni triggers Dectin-2, which activates the Nlrp3 inflammasome and alters adaptive immune responses

机译：曼氏血吸虫触发Dectin-2，后者激活Nlrp3炎性体并改变适应性免疫反应

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The propensity of helminths, such as schistosomes, to immuno-modulate the host's immune system is an essential aspect of their survival. Previous research has demonstrated how soluble schisto-somal egg antigens (SEA) dampen TLR-signaling during innate immune responses. We show here that the suppressive effect by SEA on TLR signaling is simultaneously coupled to the activation of the Nlrp3 (NLR family, pyrin domain containing 3) inflammasome and thus IL-1β production. Therefore, the responsible protein component of SEA contains the second signal that is required to trigger proteolytic pro-IL-1β processing. Moreover, the SEA component binds to the Dectin-2/FcRγ (Fc receptor γ chain) complex and activates the Syk kinase signaling pathway to induce reactive oxygen species and potassium efflux. As IL-1β has been shown to be an essential orchestrator against several pathogens we studied the in vivo consequences of Schistosoma mansoni infection in mice deficient in the central inflammasome adapter ASC and Nlrp3 molecule. These mice failed to induce local IL-1β levels in the liver and showed decreased immunopathology. Interestingly, antigen-specific Th1, Th2, and Th17 responses were down-regulated. Overall, these data imply that component(s) within SEA induce IL-1β production and unravel a crucial role of Nlrp3 during S. mansoni infection.
机译：蠕虫（如血吸虫）对宿主的免疫系统进行免疫调节的倾向是其生存的重要方面。先前的研究表明，可溶性血吸虫卵蛋白抗原（SEA）在先天免疫应答过程中如何抑制TLR信号传导。我们在这里显示SEA对TLR信号传导的抑制作用同时与Nlrp3（NLR家族，含3个吡啶结构域）炎性小体的激活相关，因此与IL-1β产生有关。因此，SEA的负责蛋白质成分包含触发蛋白水解pro-IL-1β加工所需的第二个信号。此外，SEA组分与Dectin-2 /FcRγ（Fc受体γ链）复合物结合并激活Syk激酶信号传导途径，以诱导活性氧和钾外流。由于已经证明IL-1β是抵抗几种病原体的重要协调剂，因此我们研究了曼氏血吸虫感染在缺乏中央炎症小体衔接子ASC和Nlrp3分子的小鼠中的体内后果。这些小鼠未能诱导肝脏中局部IL-1β的水平，并显示出免疫病理学降低。有趣的是，抗原特异性Th1，Th2和Th17反应被下调。总体而言，这些数据暗示SEA中的一种或多种成分诱导IL-1β的产生，并阐明曼氏葡萄球菌感染过程中Nlrp3的关键作用。

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    Manuel Ritter; Olaf Gross; Sarah Kays; Jiirgen Ruland; Falk Nimmerjahn; Shinobu Saijo; Jiirg Tschopp; Laura E. Layland; Clarissa Prazeres da Costa;

  • 作者单位

    Institute for Microbiology, Immunology and Hygiene, Technische Universitaet Muenchen, 81675 Munich, Germany;

    Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland;

    Institute for Microbiology, Immunology and Hygiene, Technische Universitaet Muenchen, 81675 Munich, Germany;

    Institute of Molecular Immunology, University Hospital rechts der Isar, Technische Universitaet Muenchen, 81675 Munich, Germany,Laboratory of Signaling in the Immune System, Helmholtz-Zentrum Muenchen-Germany, Research Center for Environmental Health, 85764 Neuherberg, Germany;

    Experimental Immunology and Immunotherapy Medical Department 3, University of Erlangen-Nuernberg, 91054 Erlangen, Germany;

    Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan;

    Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland;

    Institute for Microbiology, Immunology and Hygiene, Technische Universitaet Muenchen, 81675 Munich, Germany,Institute of Medical Microbiology, Immunology and Parasitology, University Clinic Bonn, 53105 Bonn, Germany;

    Institute for Microbiology, Immunology and Hygiene, Technische Universitaet Muenchen, 81675 Munich, Germany;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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