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Updated: Aug 21, 2026
An Ex Vivo Explant Model for Studying Glial Interactions in the Mouse Retina
Published on: July 15, 2025
CD200 maintains microglial potential to migrate in adult human retinal explant model
Debra A Carter1, Andrew D Dick
1University of Bristol, Bristol Eye Hospital, Bristol, UK.
Purpose:
Retinal microglia (MG) migrate in response to injury, degeneration and inflammation dependent upon both soluble and cognate signals they receive. Previously we found that lipopolysaccharide/interferon-gamma (LPS/IFNgamma) stimulation induces a paradoxical IL-10 mediated suppression of MG migration from retinal explants. Given the high expression of neuronal CD200, which can induce down regulation of CD200 receptor-positive MG activation and neuronal fractalkine expression potentially stimulating MG migration, we wished to further examine their respective roles in the maintenance of MG activation and migration.
Methods:
A human retinal explant model of MG migration was used. CD200 receptor and fractalkine receptor stimulation was achieved by addition to explants of CD200:Fc fusion protein and recombinant cytokine respectively, with or without LPS-IFNgamma stimulation that is known to suppress migration. Cell migration and cell activation (iNOS expression) was counted and assessed by numbers of CD45+ cells by immunofluorescence and standardised flow cytometric bead array analysis was performed for cytokine production.
Results:
Retinal explants expressed fractalkine and CX3CR1 immunohistochemically and by PCR. Addition of Fractalkine and not CD200:Fc induced MG migration from retinal explants. However LPS/IFNgamma-induced suppression of MG migration could only be restored in the presence of CD200:Fc, whilst MG remained iNOS-negative and generated IL-10.
Conclusions:
Microglial responses are tightly governed within retina. Although MG do not classically activate following LPS/IFNgamma stimulation, their migration is sustained via CD200R stimulation maintaining their potential to migrate in response to injury.
Insights
Retinal microglia (MG) migration is regulated by CD200 receptor (CD200R) stimulation, which sustains their ability to respond to injury, even when inflammation suppresses migration. This highlights CD200R
Area of Science:
- Ophthalmology
- Neuroimmunology
- Cell Biology
Background:
- Retinal microglia (MG) are crucial immune cells in the eye.
- MG migration is essential for responding to retinal injury, degeneration, and inflammation.
- Previous research indicated lipopolysaccharide/interferon-gamma (LPS/IFNgamma) paradoxically suppresses MG migration via IL-10.
- Neuronal CD200 and fractalkine signaling influence MG activation and migration.
Purpose of the Study:
- To investigate the roles of neuronal CD200 and fractalkine in regulating MG activation and migration within the retina.
- To understand how CD200 receptor (CD200R) and fractalkine signaling modulate MG responses to inflammatory stimuli like LPS/IFNgamma.
Main Methods:
- Utilized a human retinal explant model to study MG migration.
- Stimulated CD200R and fractalkine receptors using CD200:Fc fusion protein and recombinant fractalkine, respectively.
- Assessed MG migration, activation (iNOS expression), and cytokine production (IL-10) using immunofluorescence and flow cytometry, with and without LPS/IFNgamma stimulation.
Main Results:
- Retinal explants expressed fractalkine and its receptor CX3CR1.
- Fractalkine, but not CD200:Fc, directly induced MG migration.
- CD200:Fc restored LPS/IFNgamma-suppressed MG migration, while MG remained iNOS-negative and produced IL-10.
Conclusions:
- Microglial responses in the retina are tightly controlled.
- CD200R stimulation sustains MG migration potential, even under inflammatory conditions that typically suppress it.
- This sustained migration capacity is crucial for MG's ability to respond to retinal injury.
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