Abstract
The high mortality and morbidity rate of stroke is a chronic problem that plagues human society. The activation of microglia is one of the principal reasons why neuroinflammation induces cerebral dysfunction. Because of their vital functions in the regulation of neuroinflammation, microglia constitute an important target for stroke. Given that there is an innate self-preservation mechanism between neurons and microglia, the transmembrane glycoproteins on the surface of their membranes, namely CD200 and CD200R, have become a popular topic of research. Numerous studies have demonstrated that CD200-CD200R interaction, microglial activation, and poststroke neuroinflammatory damage are inextricably linked. In this review, we describe the above relationship from a new perspective. We specifically focus on neuroinflammation after stroke. The role of crosstalk of CD200-CD200R inhibitory immune ligand receptors in immune regulation will also be illustrated. Thus, we will see how poststroke injury can be influenced by the CD200-CD200R crosstalk. Finally, we will discuss the possibility of clinical application of the result of CD200-CD200R interaction to manage neuroinflammatory injury after stroke.
Highlights
Stroke with high mortality and morbidity rates have a high incidence worldwide and threatens human health and quality of life
There are no studies on the specific repair mechanisms and therapeutic effects of CD200CD200R in poststroke inflammation injury, CD200R, could still be considered as a high potential target in the study of stroke immunotherapy
The toxic damage caused to neurons by overactivated microglia far outweighs its benefits (Weinstein et al, 2010; Kanazawa et al, 2017)
Summary
Stroke with high mortality and morbidity rates have a high incidence worldwide and threatens human health and quality of life It is a devastating disease and continues to play an important role in current research in the field of medicine. Microglia/macrophages are the main immune cells in the defense against brain damage (Xiong et al, 2016). In the central nervous system, CD200R is mainly expressed in microglia (Hoek et al, 2000). Neurons are thought to have a self-protection mechanism in which they express CD200 that binds to CD200R on the microglial surface, which further prevents secondary neuronal injury caused by microglia (Hoek et al, 2000; Wang, 2010; Manich et al, 2019). This review, we have mainly focused our attention on the proinflammatory functions of microglial activation closely linked to the regulator CD200-CD200R
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