Cutting edge: Toll-like receptor signaling in macrophages induces ligands for the NKG2D receptor
Cutting edge: Toll-like receptor signaling in macrophages induces ligands for the NKG2D receptor
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DOI：
10.4049/jimmunol.172.4.2001
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发表时间：
2004-02-15
影响因子：
4.4
通讯作者：
Lanier, LL
中科院分区：
文献类型：
--
作者：
Hamerman, JA;Ogasawara, K;Lanier, LL
巨噬细胞通过使用Toll样受体（M）蛋白家族识别感染的存在，该蛋白家族检测细菌、病毒和真菌病原体上的配体。我们发现，用已知通过TLPs发出信号的病原体产物刺激的小鼠巨噬细胞表达NKG 2D受体的配体，该受体存在于NK细胞、活化的CD 8（+）T细胞和活化的巨噬细胞上。TLR信号通过MyD 88衔接子上调NKG 2D配体的视黄酸早期诱导型-1（RAE-1）家族的转录，但不上调H-60或鼠UL 16结合蛋白样转录物-1。RAE-1蛋白存在于活化但非静息巨噬细胞的表面，可通过NK细胞上的NKG 2D检测到，导致该受体在体外和体内下调。RAE-1-NKG 2D相互作用提供了一种机制，通过该机制，NK细胞和感染的巨噬细胞在对感染的先天免疫应答期间直接通信。
Macrophages recognize the presence of infection by using the Toll-like receptor (M)family of proteins that detect ligands on bacterial, viral, and fungal pathogens. We show that murine macrophages stimulated with pathogen products known to signal through TLPs express ligands for the NKG2D receptor, found on NK cells, activated CD8(+) T cells and activated macrophages. TLR signaling, through the MyD88 adaptor, up-regulates transcription of the retinoic acid early inducible-1 (RAE-1) family of NKG2D ligands, but not H-60 or murine UL16-binding protein-like transcript-1. RAE-1 proteins are found on the surface of activated, but not resting, macrophages and can be detected by NKG2D on NK cells resulting in down-regulation of this receptor both in vitro and in vivo. RAE-1-NKG2D interactions provide a mechanism by which NK cells and infected macrophages communicate directly during an innate immune response to infection.