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Restraining IL-17: Del-1 deals the blow

机译：抑制IL-17：Del-1受到打击

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摘要

The recruitment of neutrophils to sites of infection is tightly regulated to mediate host protection and to minimize pathological inflammation. The cytokine interleukin 17 (IL-17) has been well characterized as inducing granulopoietic factors such as granulocyte colony-stimulating factor (G-CSF) and CXC chemokines such as CXCL1, CXCL2 and CXCL5 to mediate the recruitment of neutrophils to sites of infection and inflammation1. Furthermore, IL-17-mediated induction of G-CSF also results in the differentiation of CD34+ progenitors into neutrophil progenitors, thereby maintaining the influx of neutrophils into chronic inflammatory sites1. Although the factors that mediate and maintain the recruitment of neutrophils during chronic inflammation have been identified, the factors that regulate and restrain the recruitment of neutrophils to limit chronic inflammation and associated disease pathogenesis are not well described. Identifying such factors will allow the design of new therapeutics to decrease chronic inflammation and the resultant disease progression. In this issue of Nature Immunology, Chavakis and colleagues identify such a molecule, Del-1 ('developmental endothelial locus 1'), and show that Del-1 inhibits IL-17 expression and suppresses the recruitment of neutrophils and the associated inflammation-mediated pathology in a model ofperiodontitis.
机译：嗜中性粒细胞向感染部位的募集受到严格调节，以介导宿主保护并最大程度地减少病理性炎症。细胞因子白介素17（IL-17）已被很好地表征为诱导粒细胞生成因子，例如粒细胞集落刺激因子（G-CSF）和CXC趋化因子，例如CXCL1，CXCL2和CXCL5，以介导嗜中性粒细胞募集到感染部位和炎症1。此外，IL-17介导的G-CSF诱导还导致CD34 +祖细胞分化为嗜中性白细胞祖细胞，从而保持嗜中性白细胞流入慢性炎症部位1。尽管已经确定了在慢性炎症过程中介导和维持嗜中性粒细胞募集的因素，但尚未很好地描述调节和限制嗜中性粒细胞募集以限制慢性炎症和相关疾病发病机理的因素。识别这些因素将允许设计新的疗法，以减少慢性炎症和由此引起的疾病进展。在本期《自然免疫学》中，Chavakis及其同事鉴定出了这样的分子Del-1（“发育的内皮基因座1”），并表明Del-1抑制IL-17表达并抑制中性粒细胞的募集以及相关的炎症介导牙周炎模型中的病理学。

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