Triggering receptor expressed on myeloid cells-1 as a new therapeutic target during inflammatory diseases.

Self/nonself Pub Date : 2010-07-01 Epub Date: 2010-07-02 DOI:10.4161/self.1.3.12891
Marc Derive, Frédéric Massin, Sébastien Gibot
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引用次数: 38

Abstract

The Triggering Receptor Expressed on Myeloid cells (TREM)-1 is a recently identified molecule involved in monocytic activation and inflammatory response. It belongs to a family related to Natural Killer cell-receptors and is expressed on neutrophils, mature monocytes and macrophages. The engagement of TREM-1 synergizes with several Toll Like Receptors (TLR) and/or NOD Like Receptors (NLR) activation in amplifying the inflammatory response mediated by microbial components or danger signals. The implication of TREM-1 during experimental models of acute or chronic inflammatory conditions, as well as during cancer, begins to understand. Furthermore, the modulation of the TREM-1 signaling pathway by the use of small synthetic peptides derived from its extracellular moiety confers interesting survival advantages during experimental murine septic shock and protects from organ damage during other inflammatory diseases. This review summarizes the recent advances on TREM-1 biology and highlights the promises of its therapeutic modulation.

髓细胞上表达的触发受体-1作为炎症性疾病的新治疗靶点。
髓样细胞触发受体(TREM)-1是最近发现的参与单核细胞活化和炎症反应的分子。它属于一个与自然杀伤细胞受体相关的家族,在中性粒细胞、成熟单核细胞和巨噬细胞上表达。TREM-1的参与与几种Toll样受体(TLR)和/或NOD样受体(NLR)的激活协同作用,放大由微生物成分或危险信号介导的炎症反应。TREM-1在急性或慢性炎症以及癌症的实验模型中的意义开始被理解。此外,通过使用由TREM-1细胞外片段衍生的小合成肽来调节TREM-1信号通路,在实验性小鼠感染性休克期间具有有趣的生存优势,并在其他炎症性疾病期间保护器官免受损害。本文综述了TREM-1生物学的最新进展,并强调了其治疗调节的前景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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