Triggering receptor expressed on myeloid cells-2 (TREM2) is an innate immune receptor that promotes phagocytosis by microglia. However, whether TREM2 is related to the stimulus-dependent phagocytic activity of microglia is unclear. In this study, the primary cultured microglia were stimulated with interferon (IFN)-γ, interleukin (IL)-4, and interleukin (IL)-10, respectively, and their phagocytic activity against microbeads and apoptotic neural stem cells (NSCs) was measured. TREM2 of microglia was detected by qPCR and western blotting. The TREM2 signal was blocked in microglia using the siRNA technique. The results showed that IL-4 or IL-10 treatment significantly increased the number of microglia gathered around the apoptotic neurosphere. IL-4 and IL-10 treatment also promoted phagocytosis of microbeads and apoptotic NSCs by primary cultured microglia. The TREM2 expression was up-regulated in IL-4- or IL-10- treated microglia. TREM2 siRNA treatment blocked the phagocytic activity of IL-4- or IL-10-treated microglia. In conclusion, these results indicated that IL-4 and IL-10 promote the phagocytic activity of microglia by the up-regulation of TREM2, which suggested a new potential therapeutic target for neurodegenerative disease.

在髓样细胞上表达的触发受体 2 (TREM2) 是一种先天免疫受体，可促进小胶质细胞的吞噬作用。然而，TREM2 是否与小胶质细胞的刺激依赖性吞噬活性有关尚不清楚。在本研究中，分别用干扰素 (IFN)-γ、白介素 (IL)-4 和白介素 (IL)-10 刺激原代培养的小胶质细胞，它们对微珠和凋亡神经干细胞 (NSC) 的吞噬活性为测量。通过qPCR和蛋白质印迹检测小胶质细胞的TREM2。使用 siRNA 技术在小胶质细胞中阻断了 TREM2 信号。结果表明，IL-4或IL-10处理显着增加了凋亡神经球周围聚集的小胶质细胞数量。IL-4 和 IL-10 处理还促进了原代培养的小胶质细胞对微珠和凋亡神经干细胞的吞噬作用。TREM2 表达在 IL-4 或 IL-10 处理的小胶质细胞中上调。TREM2 siRNA 处理阻断了 IL-4 或 IL-10 处理的小胶质细胞的吞噬活性。总之，这些结果表明 IL-4 和 IL-10 通过上调 TREM2 来促进小胶质细胞的吞噬活性，这为神经退行性疾病提供了一个新的潜在治疗靶点。