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在 GM-CSF BMDC 模型中,负责炎性小体活性的是巨噬细胞,而不是树突状细胞。

Macrophages, rather than DCs, are responsible for inflammasome activity in the GM-CSF BMDC model.

机构信息

Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.

出版信息

Nat Immunol. 2019 Apr;20(4):397-406. doi: 10.1038/s41590-019-0313-5. Epub 2019 Feb 11.

Abstract

Inflammasomes are one of the most important mechanisms for innate immune defense against microbial infection but are also known to drive various inflammatory disorders via processing and release of the cytokine IL-1β. As research into the regulation and effects of inflammasomes in disease has rapidly expanded, a variety of cell types, including dendritic cells (DCs), have been suggested to be inflammasome competent. Here we describe a major fault in the widely used DC-inflammasome model of bone marrow-derived dendritic cells (BMDCs) generated with the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF). We found that among GM-CSF bone marrow-derived cell populations, monocyte-derived macrophages, rather than BMDCs, were responsible for inflammasome activation and IL-1β secretion. Therefore, GM-CSF bone marrow-derived cells should not be used to draw conclusions about DC-dependent inflammasome biology, although they remain a useful tool for analysis of inflammasome responses in monocytes-macrophages.

摘要

炎症小体是先天免疫防御微生物感染的最重要机制之一,但也已知通过加工和释放细胞因子 IL-1β 来驱动各种炎症性疾病。随着对炎症小体在疾病中的调节和作用的研究迅速扩展,各种细胞类型,包括树突状细胞 (DC),被认为具有炎症小体能力。在这里,我们描述了一种广泛使用的细胞因子粒细胞-巨噬细胞集落刺激因子 (GM-CSF) 生成的骨髓来源树突状细胞 (BMDC) 的炎症小体模型中的一个主要缺陷。我们发现,在 GM-CSF 骨髓细胞群体中,单核细胞衍生的巨噬细胞而不是 BMDC 负责炎症小体的激活和 IL-1β 的分泌。因此,尽管 GM-CSF 骨髓细胞仍然是分析单核细胞-巨噬细胞中炎症小体反应的有用工具,但不应将其用于得出关于 DC 依赖性炎症小体生物学的结论。

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