TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria.
TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria.
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DOI：
10.1083/jcb.200808080
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发表时间：
2009-01-26
期刊：
影响因子：
--
通讯作者：
Seaman WE
中科院分区：
文献类型：
--
作者：
N'Diaye EN;Branda CS;Branda SS;Nevarez L;Colonna M;Lowell C;Hamerman JA;Seaman WE
吞噬作用是对病原体的免疫应答所必需的，它是由病原体与吞噬细胞表达的细胞表面受体之间的特异性相互作用启动的。本研究确定髓样细胞2 （TREM-2）上表达的触发受体及其信号对偶物DAP12是促进细菌吞噬的分子复合物。TREM-2-DAP12的表达使非吞噬性中国仓鼠卵巢细胞能够内化细菌。这种功能取决于肌动蛋白细胞骨架动力学和小鸟苷三磷酸酶Rac和Cdc42的活性。内化还需要src激酶活性和酪氨酸磷酸化。在骨髓源性巨噬细胞中，在缺乏DAP12的情况下，吞噬能力下降，通过表达TREM-2-DAP12可以恢复吞噬能力。TREM-2的缺失抑制了细菌的结合和摄取。最后，在syk缺陷巨噬细胞中，trem -2依赖性吞噬功能受损。这项研究强调了TREM-2-DAP12在细菌病原体免疫应答中的新作用。
Phagocytosis, which is essential for the immune response to pathogens, is initiated by specific interactions between pathogens and cell surface receptors expressed by phagocytes. This study identifies triggering receptor expressed on myeloid cells 2 (TREM-2) and its signaling counterpart DAP12 as a molecular complex that promotes phagocytosis of bacteria. Expression of TREM-2–DAP12 enables nonphagocytic Chinese hamster ovary cells to internalize bacteria. This function depends on actin cytoskeleton dynamics and the activity of the small guanosine triphosphatases Rac and Cdc42. Internalization also requires src kinase activity and tyrosine phosphorylation. In bone marrow–derived macrophages, phagocytosis is decreased in the absence of DAP12 and can be restored by expression of TREM-2–DAP12. Depletion of TREM-2 inhibits both binding and uptake of bacteria. Finally, TREM-2–dependent phagocytosis is impaired in Syk-deficient macrophages. This study highlights a novel role for TREM-2–DAP12 in the immune response to bacterial pathogens.
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