The role of N-glycosylation of CD200-CD200R1 interaction in classical microglial activation.

ABSTRACT: BackgroundMicroglial 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.ResultsCD200R1 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-1? and TNF-?.ConclusionN44 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.Electronic supplementary materialThe online version of this article (10.1186/s12950-018-0205-8) contains supplementary material, which is available to authorized users.

SUBMITTER: Liu C 

PROVIDER: S-EPMC6300008 | biostudies-other | 2018

REPOSITORIES: biostudies-other