IL-4 and IL-10 promotes phagocytic activity of microglia by up-regulation of TREM2
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ORIGINAL ARTICLE
IL-4 and IL-10 promotes phagocytic activity of microglia by up-regulation of TREM2 Saini Yi . Xue Jiang . Xiaofang Tang . Yahui Li . Chenghong Xiao . Jinqiang Zhang . Tao Zhou
Received: 18 September 2019 / Accepted: 26 June 2020 Ó Springer Nature B.V. 2020
Abstract 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)-c, 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 upregulated 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 S. Yi X. Tang Y. Li C. Xiao J. Zhang T. Zhou (&) Guizhou University of Traditional Chinese Medicine, Guiyang 550025, China e-mail: [email protected]; [email protected] X. Jiang University of Macau, Macau 999078, China
phagocytic activity of microglia by the up-regulation of TREM2, which suggested a new potential therapeutic target for neurodegenerative disease. Keywords TREM2
Microglia Phagocytosis IL-4 IL-10
Introduction Microglia are the resident immune cells of the central nervous system (CNS) that play an immunoregulatory role by phagocytosis of protein aggregates and cell fragments, thus maintaining the stability of the central nervous system (Loane and Kumar 2016). Impaired microglial functions are thought to be involved in the onset and progression of various neurodevelopmental and neurodegenerative diseases (Walker and Lue 2015). Studies have shown that microglia exhibit clear stimulation-dependent phenotypic and functional consequences (Hanisch 2002). The pro-inflammatory cytokines (IFN-c, IL-b, TNF-a) polarize microglia cells toward the M1 phenotype, and consequently aggravates neuropathology and accelerates pathological process (Gordon and Taylor 2005). The anti-inflammatory cytokines (IL-4, IL-10) polarize microglia cells toward the M2 phenotype which plays a key role in neuroprotection and tissue repair (Gensel and Zhang 2015; Orihuela et al. 2016; Schulz et al.
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Cytotechnology
2019). The phagocytic activity of microglia is also regulated by cytokines. The phagocytic function of microglia plays an important role in neurological diseases such as Alzheimer’s dis
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