Iwai Hideyuki, Kohsaka Hitoshi
Department of Medicine and Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University.
Nihon Rinsho Meneki Gakkai Kaishi. 2012;35(1):81-6. doi: 10.2177/jsci.35.81.
Triggering receptor expressed on myeloid cells (TREM)-1 belongs to an immunoglobulin super family and is expressed on neutrophils, mature monocytes and macrophages. The engagement of TREM-1 synergizes with several Toll Like Receptors (TLR) activation in amplifying the inflammatory response. TREM-1 blockade using a fusion protein containing murine TREM-1 extracellular domain and human immunoglobulin Fc portion was reported to prevent death in mouse models of microbial peritonitis and protect from organ damage during other inflammatory diseases. There are many reports suggesting the involvement of TREM-1 in the pathogenesis of rheumatoid arthritis. Blockade of TREM-1 could be a new therapeutic target in rheumatoid arthritis without impairing the host defense against microbes. In this report, we outline the role of TREM-1 and the trial of developing anti-rheumatic drugs by targeting its ligand.
髓系细胞触发受体（TREM）-1属于免疫球蛋白超家族，表达于中性粒细胞、成熟单核细胞和巨噬细胞上。TREM-1的激活与多种Toll样受体（TLR）协同作用，放大炎症反应。据报道，使用含鼠TREM-1胞外域和人免疫球蛋白Fc部分的融合蛋白阻断TREM-1可防止小鼠微生物性腹膜炎模型死亡，并在其他炎症性疾病中保护器官免受损伤。有许多报道提示TREM-1参与类风湿关节炎的发病机制。阻断TREM-1可能成为类风湿关节炎的一个新治疗靶点，而不损害宿主对微生物的防御。在本报告中，我们概述了TREM-1的作用以及通过靶向其配体开发抗风湿药物的试验。
