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Microglial expression of CD83 governs cellular activation and restrains neuroinflammation in experimental autoimmune
Pia Sinner1, Katrin Peckert-Maier1, Hashem Mohammadian2
1Department of Immune Modulation, Uniklinikum Erlangen, Friedrich-Alexander Universität Erlangen-Nürnberg, 91052, Erlangen, Germany.
Abstract:
Microglial activation during neuroinflammation is crucial for coordinating the immune response against neuronal tissue, and the initial response of microglia determines the severity of neuro-inflammatory diseases. The CD83 molecule has been recently shown to modulate the activation status of dendritic cells and macrophages. Although the expression of CD83 is associated with early microglia activation in various disease settings, its functional relevance for microglial biology has been elusive. Here, we describe a thorough assessment of CD83 regulation in microglia and show that CD83 expression in murine microglia is not only associated with cellular activation but also with pro-resolving functions. Using single-cell RNA-sequencing, we reveal that conditional deletion of CD83 results in an over-activated state during neuroinflammation in the experimental autoimmune encephalomyelitis model. Subsequently, CD83-deficient microglia recruit more pathogenic immune cells to the central nervous system, deteriorating resolving mechanisms and exacerbating the disease. Thus, CD83 in murine microglia orchestrates cellular activation and, consequently, also the resolution of neuroinflammation.
Insights
CD83 protein in microglia is vital for controlling neuroinflammation and promoting resolution. Its absence leads to over-activated microglia, increased immune cell infiltration, and worsened disease severity in the central nervous system.
Area of Science:
- Neuroimmunology
- Cellular Biology
- Molecular Medicine
Background:
- Microglial activation is central to neuroinflammation and disease progression.
- The CD83 molecule regulates immune cell activation but its role in microglia is unclear.
- CD83 expression correlates with early microglial activation in disease.
Purpose of the Study:
- To investigate the functional role of CD83 in microglial activation and neuroinflammation.
- To assess CD83's impact on the resolution of neuroinflammatory responses.
- To understand CD83's contribution to microglial-mediated immune responses in the central nervous system.
Main Methods:
- Single-cell RNA-sequencing to analyze microglial gene expression.
- Conditional deletion of CD83 in murine models.
- Assessment of neuroinflammation in the experimental autoimmune encephalomyelitis model.
Main Results:
- CD83 expression in microglia is linked to both activation and pro-resolving functions.
- Conditional CD83 deletion leads to microglial over-activation during neuroinflammation.
- CD83 deficiency exacerbates experimental autoimmune encephalomyelitis by increasing pathogenic immune cell recruitment.
Conclusions:
- CD83 orchestrates microglial activation and the resolution of neuroinflammation.
- Targeting CD83 may offer therapeutic strategies for neuro-inflammatory diseases.
- CD83 plays a critical role in balancing immune responses within the central nervous system.
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