Background Microglial inflammatory activation is the common feature of the central nervous system (CNS) diseases. Microglia can be activated and particularly polarized toward a dual role in the injured CNS. The CD200 receptor 1 (CD200R1) inhibits inflammatory microglia activation as illustrated by studies. Publications show abnormal activation of microglia secondary to the deficient inhibit of CD200-CD200R interaction. In the present study, we established a neuronal-microglia co-culture system to investigate the association between CD200R1 engagement and classical microglial activation. We analyzed the glycosylation of CD200R1 and the CD200 binding. Secretion of pro-inflammatory cytokines were measured. Results CD200R1 was N-glycosylated at Asparagine 44 (Asn44, N44). Mutation of this site disrupted CD200-CD200R1 interaction and up-regulated the expression of cytokines iNOS, CD86, IL-1β and TNF-α. Conclusion N44 of CD200R1 is a significant binding site for CD200-CD200R1 interaction and play a critical role in the maintenance of microglia. The N-glycosylation of CD200R1 could serve as a therapeutic agent for CNS inflammation.

中文翻译：

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CD200-CD200R1 相互作用的 N-糖基化在经典小胶质细胞活化中的作用。

背景小胶质细胞炎症激活是中枢神经系统（CNS）疾病的共同特征。小胶质细胞可以被激活，特别是在受损的中枢神经系统中发挥双重作用。如研究所示，CD200 受体 1 (CD200R1) 抑制炎症性小胶质细胞活化。出版物显示继发于 CD200-CD200R 相互作用抑制不足的小胶质细胞异常激活。在本研究中，我们建立了一个神经元-小胶质细胞共培养系统来研究 CD200R1 参与与经典小胶质细胞激活之间的关联。我们分析了 CD200R1 的糖基化和 CD200 结合。测量促炎细胞因子的分泌。结果 CD200R1 在天冬酰胺 44 (Asn44, N44) 处被 N-糖基化。该位点的突变破坏了 CD200-CD200R1 相互作用并上调了细胞因子 iNOS、CD86、IL-1β 和 TNF-α 的表达。结论 CD200R1的N44是CD200-CD200R1相互作用的重要结合位点，在小胶质细胞的维持中起关键作用。CD200R1 的 N-糖基化可作为 CNS 炎症的治疗剂。