Microglial expression of CD83 governs cellular activation and restrains neuroinflammation in experimental autoimmune encephalomyelitis

Pia Sinner, Katrin Peckert-Maier, Hashem Mohammadian, Christine Kuhnt, Christina Draßner, Vasiliki Panagiotakopoulou, Simon Rauber, Mathias Linnerbauer, Zhana Haimon, Dmytro Royzman, Deborah Kronenberg-Versteeg, Andreas Ramming, Alexander Steinkasserer and Andreas B. Wild ()
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Pia Sinner: Friedrich-Alexander Universität Erlangen-Nürnberg
Katrin Peckert-Maier: Friedrich-Alexander Universität Erlangen-Nürnberg
Hashem Mohammadian: Friedrich-Alexander Universität Erlangen-Nürnberg
Christine Kuhnt: Friedrich-Alexander Universität Erlangen-Nürnberg
Christina Draßner: Friedrich-Alexander Universität Erlangen-Nürnberg
Vasiliki Panagiotakopoulou: University of Tübingen
Simon Rauber: Friedrich-Alexander Universität Erlangen-Nürnberg
Mathias Linnerbauer: Friedrich-Alexander Universität Erlangen-Nürnberg
Zhana Haimon: Weizmann Institute of Science
Dmytro Royzman: Friedrich-Alexander Universität Erlangen-Nürnberg
Deborah Kronenberg-Versteeg: University of Tübingen
Andreas Ramming: Friedrich-Alexander Universität Erlangen-Nürnberg
Alexander Steinkasserer: Friedrich-Alexander Universität Erlangen-Nürnberg
Andreas B. Wild: Friedrich-Alexander Universität Erlangen-Nürnberg

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: 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.

Date: 2023
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DOI: 10.1038/s41467-023-40370-2

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