ArticleCNS neuroscience & therapeutics2024
CD22 blockade aggravates EAE and its role in microglia polarization.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TrkB promotes the neuronal secretion of soluble Siglec-2 (CD22) to mitigate microglial activation and alleviate depression-like behaviors in male mice.Molecular psychiatry · 2026Article
- Microglial ITAM & ITIM Signaling in Neurodegenerative Disease and Brain Aging.Journal of molecular biology · 2026Review
- B cell-specific METTL3 depletion exacerbates experimental autoimmune encephalomyelitis.Cellular and molecular life sciences : CMLS · 2026Article
- Immunological and pathological roles of Siglecs: a molecular review.Frontiers in immunology · 2026Review
- CD22 blockade aggravates EAE and its role in microglia polarization.CNS neuroscience & therapeutics · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
aimsMultiple 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.
methodsExperimental 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.
resultsWe 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.
conclusionCollectively, 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.
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Registered trials
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