Abstract Background Opsonization, is the molecular mechanism by which target molecules promote interactions with phagocyte cell surface receptors to remove unwanted cells by induced phagocytosis. We designed an in vitro system to demonstrate that this procedure could be driven to eliminate adipocytes, using peptides mimicking regions of the complement protein C3b to promote opsonization and enhance phagocytosis. Two cell lines were used: 1) THP-1 monocytes differentiated to macrophages, expressing the C3b opsonin receptor CR1 in charge of the removal of unwanted coated complexes; 2) 3T3-L1 fibroblasts differentiated to adipocytes, expressing AQP7, to evaluate the potential of peptides to stimulate opsonization. 3) A co-culture of the two cell lines to demonstrate that phagocytosis could be driven to cell withdrawal with high efficiency and specificity. Results An array of peptides were designed and chemically synthesized. p3691 and p3931 joined bound to the CR1 receptor activating phagocytosis (p Conclusions This in vitro model could help understanding the receptor-ligand interaction in the withdrawal of unwanted macromolecules in vivo. The adipocyte-phagocytosis discussed may help to control obesity, since peptides of C3b stimulated the CR1 receptor, promoting opsonisation and phagocytosis of lipid-containing structures, and recognition of AQP7 in the differentiated adipocytes, favored the phagocytic activity of macrophages, robustly supported by the co-culture strategy.

中文翻译：

---

模拟补体系统的体外模型有利于对不需要的细胞进行定向吞噬

摘要背景调理作用是靶分子促进与吞噬细胞表面受体相互作用以通过诱导吞噬作用去除不需要的细胞的分子机制。我们设计了一个体外系统来证明该程序可以用来消除脂肪细胞，使用模拟补体蛋白 C3b 区域的肽来促进调理作用和增强吞噬作用。使用了两种细胞系：1) THP-1 单核细胞分化为巨噬细胞，表达 C3b 调理素受体 CR1，负责去除不需要的包被复合物；2) 3T3-L1 成纤维细胞分化为脂肪细胞，表达 AQP7，以评估肽刺激调理作用的潜力。3) 两种细胞系的共培养，以证明吞噬作用可以高效和特异性地驱动细胞退出。结果 设计并化学合成了一系列肽。p3691 和 p3931 与 CR1 受体结合，激活吞噬作用（p 结论）这种体外模型有助于理解体内不需要的大分子撤回中的受体-配体相互作用。所讨论的脂肪细胞吞噬作用可能有助于控制肥胖，因为 C3b 的肽刺激 CR1 受体，促进含脂质结构的调理作用和吞噬作用，以及在分化的脂肪细胞中识别 AQP7，有利于巨噬细胞的吞噬活性，这得到了共培养策略的有力支持。