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Related Experiment Video

Updated: Jun 26, 2025

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
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CD22 blockade aggravates EAE and its role in microglia polarization.

Weiwei Xiang1, Kan Wang1, Lu Han1

  • 1Department of Neurology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

CNS Neuroscience & Therapeutics
|May 13, 2024
PubMed
Summary

CD22 blockade worsens experimental autoimmune encephalomyelitis (EAE) in mice by promoting M1 microglial polarization, suggesting CD22 is protective against this neuroinflammatory disease.

Keywords:
CD22EAESiglecmicrogliamultiple sclerosis

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Area of Science:

  • Neuroimmunology
  • Microglial biology

Background:

  • Multiple sclerosis (MS) is a neuroinflammatory demyelinating disease.
  • Microglia play a role in MS pathogenesis, but key regulatory molecules remain unknown.

Purpose of the Study:

  • To investigate the role of CD22 in microglial activation and experimental autoimmune encephalomyelitis (EAE).

Main Methods:

  • CD22 expression in microglia was analyzed in EAE mice.
  • In vitro studies examined lipopolysaccharide-induced CD22 upregulation and CD22 blockade effects on microglial polarization.
  • In vivo studies assessed the impact of CD22 blockade on EAE severity.

Main Results:

  • Microglial CD22 expression increased in EAE mice.
  • CD22 blockade modulated microglial polarization towards the M1 phenotype.
  • CD22 blockade aggravated EAE and promoted M1 microglial polarization in vivo.

Conclusions:

  • CD22 appears to be protective against EAE.
  • CD22 plays a critical role in maintaining immune homeostasis in EAE models.