ArticleJournal of neuroinflammation2024
CD22 blockade exacerbates neuroinflammation in Neuromyelitis optica spectrum disorder.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Selective inhibition of TLR2 stimulates the maturation of oligodendroglial progenitor cells to oligodendrocytes.NeuroImmune pharmacology and therapeutics · 2026Article
- Ferritin-ApoE nanocarrier for targeted therapy of neuromyelitis optica spectrum disorder in mice.Journal of neuroinflammation · 2026Article
- Systems biology-based drug repurposing for neuroinflammation treatment in activated human microglia.Scientific reports · 2026Article
- Integrated Blood Inflammatory Ratios and Cerebrospinal Fluid Blood‒Brain Barrier Dysfunction Predict Relapse Risk in Neuromyelitis Optica Spectrum Disorder.Brain and behavior · 2026Article
- Temporal Dynamics of APOE and TREM2 Expression in Microglial Activation of NMOSD Mouse Models.Molecular neurobiology · 2025Article
- Intravitreal delivery of NMO-IgG causes primary retinal damage in the absence of optic nerve injury.Journal of neuroinflammation · 2025Article
- Lactate accumulation from HIF-1α-mediated PMN-MDSC glycolysis restricts brain injury after acute hypoxia in neonates.Journal of neuroinflammation · 2025Article
- The Role of miR-30d-5p in Neutrophil-Derived Exosomes in Promoting Systemic Lupus Erythematosus.International journal of general medicine · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundNeuromyelitis optica spectrum disorder (NMOSD) is an autoantibody-triggered central nervous system (CNS) demyelinating disease that primarily affects the spinal cord, optic nerves and brainstem. Among the first responders to CNS injury, microglia are prominent players that drive NMOSD lesion formation. However, the key molecular switches controlling the detrimental activity of microglia in NMOSD are poorly understood. CD22 governs the activity of innate and adaptive immunity. In this study, we investigated to what extent and by what mechanisms CD22 may modulate microglial activity, neuroinflammation and CNS lesion formation.
methodsTo determine the expression profile of CD22 in NMOSD, we performed single-cell sequencing and flow cytometry analysis of immune cells from human peripheral blood. We investigated the potential effects and mechanisms of CD22 blockade on microglial activity, leukocyte infiltration and CNS demyelination in a mouse model of NMOSD induced by injection of NMOSD patient serum-derived AQP4-IgG and human complement.
resultsSingle-cell sequencing and flow cytometry analysis revealed that CD22 was expressed in B cells, neutrophils, monocytes and microglia-derived exosomes in human peripheral blood from NMOSD patients and controls (n = 5 per group). In a mouse model of NMOSD, CD22 was expressed in B cells, neutrophils, monocytes and microglia (n = 8 per group). In NMOSD mice, CD22 blockade significantly increased the number of CNS lesions, astrocyte loss and demyelination, accompanied by increased inflammatory activity and phagocytosis in microglia. Furthermore, the detrimental effects of CD22 blockade were significantly alleviated in NMOSD mice subjected to depletion of microglia or Gr-1
conclusionsOur findings revealed a previously unrecognized role of CD22 as a key molecular switch that governs the detrimental effects of microglia and Gr-1
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