在髓样单核细胞中截断去泛素化酶 CYLD 的结构域可减弱炎症反应。
Truncation of the deubiquitinating domain of CYLD in myelomonocytic cells attenuates inflammatory responses.
机构信息
School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Macedonia, Greece.
出版信息
PLoS One. 2011 Jan 20;6(1):e16397. doi: 10.1371/journal.pone.0016397.
The cylindromatosis tumor suppressor (CYLD) is a deubiquitinating enzyme that has been implicated in various aspects of adaptive and innate immune responses. Nevertheless, the role of CYLD in the function of specific types of immune cells remains elusive. In this report we have used conditional gene targeting in mice to address the role of the deubiquitinating activity of CYLD in the myelomonocytic lineage. Truncation of the deubiquitinating domain of CYLD specifically in myelomonocytic cells impaired the development of lethal LPS-induced endotoxic shock and the accumulation of thioglycollate-elicited peritoneal macrophages. Our data establish CYLD as a regulator of monocyte-macrophage activation in response to inflammatory stimuli and identify it as a potential target for therapeutic intervention in relevant inflammatory disorders in humans.
圆柱瘤病抑制因子（CYLD）是一种去泛素化酶，参与适应性和先天免疫反应的各个方面。然而，CYLD 在特定类型免疫细胞功能中的作用仍不清楚。在本报告中，我们使用条件性基因靶向敲除小鼠来研究 CYLD 的去泛素化酶活性在髓系细胞中的作用。髓系细胞特异性敲除 CYLD 的去泛素化结构域会损害致死性 LPS 诱导的内毒素休克和巯基乙醇酸盐诱导的腹腔巨噬细胞积聚的发展。我们的数据表明 CYLD 是对炎症刺激产生反应的单核细胞-巨噬细胞激活的调节因子，并将其确定为人类相关炎症性疾病治疗干预的潜在靶点。
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