TNF-α-dependerit loss of IKKβ-deficient myeloid progenitors triggers a cytokine loop culminating in granulocytosis

Arun K. Mankan; Ozge Canli; Sarah Schwitalla; Paul Ziegler; Jurg Tschopp; Thomas Korn; Florian R. Greten

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TNF-α-dependerit loss of IKKβ-deficient myeloid progenitors triggers a cytokine loop culminating in granulocytosis

机译：IKKβ缺乏的髓样祖细胞的TNF-α依赖性丧失触发细胞因子环最终导致粒细胞增多

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Loss of IkB kinase (IKK) β-dependent NF-kB signaling in hemato-poietic cells is associated with increased granulopoiesis. Here we identify a regulatory cytokine loop that causes neutrophilia in /KKβ-deficient mice. TNF-α-dependent apoptosis of myeloid progenitor cells leads to the release of IL-1β, which promotes Th17 polarization of peripheral CD4~+ T cells. Although the elevation of IL-17 and the consecutive induction of granulocyte colony-stimulating factor compensate for the loss of myeloid progenitor cells, the facilitated induction of Th17 cells renders Ikkβ-deficient animals more susceptible to the development of experimental autoimmune encephalitis. These results unravel so far unanticipated direct and indirect functions for IKKβ in myeloid progenitor survival and maintenance of innate and Th17 immunity and raise concerns about long-term IKKp inhibition in IL-17-mediated diseases.

机译：造血细胞中IkB激酶（IKK）β依赖性NF-kB信号的丢失与粒细胞生成的增加有关。在这里，我们确定了在/KKβ缺陷型小鼠中引起嗜中性粒细胞增多的调节性细胞因子环。依赖于TNF-α的髓样祖细胞凋亡导致IL-1β释放，从而促进外周CD4〜+ T细胞的Th17极化。尽管IL-17的升高和粒细胞集落刺激因子的连续诱导补偿了骨髓祖细胞的损失，但Th17细胞的诱导诱导使Ikkβ缺陷型动物更容易患上实验性自身免疫性脑炎。这些结果揭示了迄今为止IKKβ在髓样祖细胞生存和维持先天免疫和Th17免疫中所未预期的直接和间接功能，并引起了人们对IL-17介导的疾病长期抑制IKKp的关注。

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《Proceedings of the National Academy of Sciences of the United States of America》 |2011年第16期|p.6567-6572|共6页
作者
Arun K. Mankan; Ozge Canli; Sarah Schwitalla; Paul Ziegler; Jurg Tschopp; Thomas Korn; Florian R. Greten;
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作者单位

Institute of Molecular Immunology, Klinikum Rechts der Isar, Technical University Munich, 81675 Munich, Germany;

Institute of Molecular Immunology, Klinikum Rechts der Isar, Technical University Munich, 81675 Munich, Germany;

Institute of Molecular Immunology, Klinikum Rechts der Isar, Technical University Munich, 81675 Munich, Germany;

Institute of Molecular Immunology, Klinikum Rechts der Isar, Technical University Munich, 81675 Munich, Germany;

Department of Biochemistry, Center of Immunity and Infection, University of Lausanne, CH-1066 Epalinges, Switzerland;

Department of Neurology, Klinikum Rechts der Isar, Technical University Munich, 81675 Munich, Germany;

Institute of Molecular Immunology, Klinikum Rechts der Isar, Technical University Munich, 81675 Munich, Germany;

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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);
原文格式 PDF
正文语种 eng
中图分类
关键词
cd34; il-7r; ikkβ inhibitor;

机译：cd34;il-7r;ikkβ抑制剂;

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1. Differential expression of Id genes in multipotent myeloid progenitor cells: Id-1 is induced by early-and late-acting cytokines while Id-2 is selectively induced by cytokines that drive terminal granulocytic differentiation. [J] . Cooper CL, Newburger PE Journal of cellular biochemistry. . 1998,第2期

机译：Id基因在多能骨髓祖细胞中的差异表达：Id-1由早期和晚期作用的细胞因子诱导，而Id-2由驱动终末粒细胞分化的细胞因子选择性诱导。
2. Ascorbic Acid, Inflammatory Cytokines (IL-1β/TNF-α/IFN-γ), or Their Combination’s Effect on Stemness, Proliferation, and Differentiation of Gingival Mesenchymal Stem/Progenitor Cells [J] . Karim M. Fawzy El-Sayed, Nhung Nguyen, Christof E. D?rfer Stem cells international . 2020,第4期

机译：抗坏血酸，炎症细胞因子（IL-1β/ TNF-α/ IFN-γ），或它们的组合对牙龈间充质茎/祖细胞的茎秆，增殖和分化的影响
3. IKK promotes cytokine-induced and cancer-associated AMPK activity and attenuates phenformin-induced cell death in LKB1-deficient cells [J] . Antonia Ricardo J., Baldwin Albert S. Science Signaling . 2018,第538期

机译：IKK促进细胞因子诱导和癌症相关的AMPK活性，并在LKB1缺陷细胞中衰减苯甲酸诱导的细胞死亡
4. Chronic Interleukin-1 Exposure Triggers Selective Expansion of Cebpa-Deficient Multipotent Hematopoietic Progenitors [D] . Higa, Kelly Chiemi. 2020

机译：慢性白细胞介素-1曝光触发CEBPA缺陷的多能造血祖细胞的选择性扩增
5. TNF-α–dependent loss of IKKβ-deficient myeloid progenitors triggers a cytokine loop culminating in granulocytosis [O] . Arun K. Mankan, Ozge Canli, Sarah Schwitalla, 2011

机译：依赖于TNF-α的IKKβ缺陷型髓样祖细胞的丢失触发了细胞因子环最终导致粒细胞增多
6. TNF-α–dependent loss of IKKβ-deficient myeloid progenitors triggers a cytokine loop culminating in granulocytosis [O] . Mankan, Arun K., Canli, Ozge, Schwitalla, Sarah, 2011

机译：IKKβ缺乏的髓样祖细胞的TNF-α依赖性丧失触发细胞因子环，最终导致粒细胞增多

TNF-α-dependerit loss of IKKβ-deficient myeloid progenitors triggers a cytokine loop culminating in granulocytosis

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