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EBI2 - Sensor for dihydroxycholesterol gradients in neuroinflammation.
Florian C Kurschus1, Florian Wanke1
1Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Biochimie
|April 25, 2018
Summary
Immune cells use Epstein-Barr virus-induced gene 2 (EBI2) to sense dihydroxycholesterols, guiding them during neuroinflammation. This sensing mechanism is upregulated in multiple sclerosis models, affecting T cell infiltration in the central nervous system.
Area of Science:
- Biochemistry
- Immunology
- Neuroscience
Background:
- Dihydroxycholesterols (e.g., 7α,25-OHC) are cholesterol metabolites produced by specific enzymes.
- These oxysterols are involved in both normal physiological states and inflammatory conditions.
- The G-protein coupled receptor (GPCR) EBI2 (GPR183) acts as a sensor for these dihydroxycholesterols.
Purpose of the Study:
- To review the role of dihydroxysterol sensing by immune cells in neuroinflammation.
- To discuss the function of EBI2 in immune cell migration in the context of central nervous system inflammation.
- To highlight the relevance of this pathway in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis.
Main Methods:
- Literature review focusing on dihydroxysterols, EBI2, and neuroinflammation.
- Analysis of studies investigating EBI2-mediated immune cell chemotaxis.
- Examination of research on EBI2 and oxysterol upregulation in EAE models.
Main Results:
- EBI2 activation by dihydroxysterols drives immune cell migration towards ligand gradients.
- Dihydroxycholesterol ligands are elevated in the CNS during EAE.
- EBI2 signaling promotes the infiltration of encephalitogenic T cells into the CNS in EAE.
Conclusions:
- Immune cell sensing of dihydroxysterols via EBI2 is a significant factor in neuroinflammation.
- This pathway contributes to the early stages of central nervous system inflammation by facilitating T cell entry.
- Understanding the dihydroxysterol-EBI2 axis offers insights into potential therapeutic targets for neuroinflammatory diseases like multiple sclerosis.
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