Nogo receptor expression in microglia/macrophages during experimental autoimmune encephalomyelitis progression

Neural Regen Res, 2018 · DOI: 10.4103/1673-5374.232488 · Published: May 1, 2018

Simple Explanation

Myelin-associated inhibitory factors in the central nervous system hinder axonal regeneration after injury. Nogo receptor 1 (NgR1) limits axonal regrowth. Microglia/macrophages are immune cells contributing to inflammatory demyelinating lesions in multiple sclerosis (MS). This study examines the role of nogo receptors in these cells during experimental autoimmune encephalomyelitis (EAE). The study found that NgR1-dependent microglial/macrophage activity did not govern the dynamics of these cell populations during EAE progression, but NgR3 may be important for myelin phagocytosis.

Study Duration

Not specified

Participants

68 ngr1+/+ and 51 ngr1–/– female mice

Evidence Level

Not specified

Key Findings

1
A significant difference in microglia/macrophage numbers between ngr1+/+ and ngr1–/– mice was identified during EAE progression, but this difference was unrelated to NgR expression on these cells.
2
Phagocytic activity of microglia/macrophages with myelin debris was enhanced in ngr1–/– mice as EAE progressed.
3
There was a modulation from a predominant M1-pathogenic to the M2-neurotrophic cell phenotype in the ngr1–/– mice during EAE progression.

Research Summary

This study investigated the expression of Nogo receptors (NgR) within microglia/macrophage populations during the progression of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). The researchers found that NgR1-dependent microglial/macrophage activity did not govern the dynamics of these cell populations during EAE progression. However, NgR3 may be an important component of myelin phagocytosis. The study suggests that CNS-specific macrophages and microglia of ngr1–/– mice may exhibit an enhanced capacity to clear inhibitory molecules that are sequestered in inflammatory lesions.

Practical Implications

Targeting NgR3

Specifically targeting NgR3 expression during EAE progression may limit the pathogenic activity of M1 macrophages/microglia.

Myelin Debris Clearance

Enhanced phagocytic clearance of myelin, influenced by NgR1 and NgR3 expression, could be a therapeutic target.

M1/M2 Polarization

Modulating microglia/macrophage polarization towards the M2 phenotype could be beneficial in neuroinflammatory conditions.

Study Limitations

1
Microglial cell specific deletion of NgR and/or its homologs was not achieved during the induction and progression of EAE.
2
The mechanism by which NgR3 can influence microglial/macrophage activity during neuroinflammation needs to be specifically addressed.
3
The collaborative interaction between NgR1/NgR3, although implied in this study, may argue that specifically targeting NgR3 expression during EAE progression may limit the pathogenic activity of M1 macrophages/microglia

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