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.
Aims:
Multiple sclerosis (MS) is a neuroinflammatory demyelinating disease. Microglia are reportedly involved in the pathogenesis of MS. However, the key molecules that control the inflammatory activity of microglia in MS have not been identified.
Methods:
Experimental autoimmune encephalomyelitis (EAE) mice were randomized into CD22 blockade and control groups. The expression levels of microglial CD22 were measured by flow cytometry, qRT-PCR, and immunofluorescence. The effects of CD22 blockade were examined via in vitro and in vivo studies.
Results:
We detected increased expression of microglial CD22 in EAE mice. In addition, an in vitro study revealed that lipopolysaccharide upregulated the expression of CD22 in microglia and that CD22 blockade modulated microglial polarization. Moreover, an in vivo study demonstrated that CD22 blockade aggravated EAE in mice and promoted microglial M1 polarization.
Conclusion:
Collectively, our study indicates that CD22 may be protective against EAE and may play a critical role in the maintenance of immune homeostasis in EAE mice.
Insights
CD22 blockade worsens experimental autoimmune encephalomyelitis (EAE) in mice by promoting M1 microglial polarization, suggesting CD22 is protective against this neuroinflammatory disease.
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.
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