Chen Mingzhuang, Tse Gary, Wong Wing Tak
School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China.
State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Hong Kong, China.
Clin Exp Pharmacol Physiol. 2021 Jan;48(1):129-136. doi: 10.1111/1440-1681.13399. Epub 2020 Sep 17.
Interleukin-4 (IL-4) signalling pathways regulate the activity of macrophages, enhance their proteolytic capacity and drive resolution of inflammation during tissue repair. The aim of this study was to examine whether IL-4 can enhance phagocytosis of necrotic cells and elucidate the molecular mechanisms.
Phagocytosis of necrotic thymocytes by RAW264.7 cells, a macrophage cell line, with or without IL-4 treatment, was determined by flow cytometry. Protein expression was determined by western blot analysis.
The phagocytosis index was significantly increased by IL-4 (10 ng/mL). IL-4-enhanced phagocytosis was mediated by upregulation of scavenger receptor CD36. STAT6 activation is required for IL-4-mediated phagocytosis.
Interleukin-4 can accelerate cell debris clearance by stimulating expression of CD36, which requires downstream STAT6 activation. Its beneficial effects on driving tissue repair and regeneration should be explored in future studies.
白细胞介素-4（IL-4）信号通路调节巨噬细胞的活性，增强其蛋白水解能力，并在组织修复过程中促进炎症消退。本研究的目的是检验IL-4是否能增强对坏死细胞的吞噬作用，并阐明其分子机制。
通过流式细胞术测定巨噬细胞系RAW264.7细胞在有或无IL-4处理情况下对坏死胸腺细胞的吞噬作用。通过蛋白质印迹分析确定蛋白质表达。
IL-4（10 ng/mL）显著提高了吞噬指数。IL-4增强的吞噬作用是由清道夫受体CD36的上调介导的。IL-4介导的吞噬作用需要STAT6激活。
白细胞介素-4可通过刺激CD36的表达来加速细胞碎片清除，这需要下游STAT6激活。其在促进组织修复和再生方面的有益作用应在未来研究中加以探索。
