ArticleScience translational medicine2021
The CD22-IGF2R interaction is a therapeutic target for microglial lysosome dysfunction in Niemann-Pick type C.
Article in Science translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 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
- Aurka-Bhlhe41 axis prevents premature aging-like microglial dysfunction and promotes remyelination.Nature communications · 2026Article
- Immunological and pathological roles of Siglecs: a molecular review.Frontiers in immunology · 2026Review
- CD22 regulates Aβ clearance in microglia through INPP5D signaling.Frontiers in cellular neuroscience · 2026Article
- Generation of Donor-Specific iPSC for Modelling Lysosomal Storage Disorders.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Neuroimaging Findings in Children and Young Adults With Neurotoxicity After CAR T-Cell Therapy for B-Cell Malignancies.Neurology · 2025Article
- Regional and aging-specific cellular architecture of non-human primate brains.Genome medicine · 2025Article
- Peripheral and central neuroimmune mechanisms in Alzheimer's disease pathogenesis.Molecular neurodegeneration · 2025Review
- CD22 modulation alleviates amyloid β-induced neuroinflammation.Journal of neuroinflammation · 2025Article
- Pretreatment level of serum sialic acid predicts both qualitative and quantitative bone metastases of prostate cancer.Frontiers in endocrinology · 2024Review
- Therapeutic potential to target sialylation and SIGLECs in neurodegenerative and psychiatric diseases.Frontiers in neurology · 2024Review
- CD22 CAR T-cell associated hematologic toxicities, endothelial activation and relationship to neurotoxicity.Journal for immunotherapy of cancer · 2023Article
- Aging microglia.Cellular and molecular life sciences : CMLS · 2023Review
- Exploring Pro-Inflammatory Immunological Mediators: Unraveling the Mechanisms of Neuroinflammation in Lysosomal Storage Diseases.Biomedicines · 2023Review
- Human sialoglycan ligands for immune inhibitory Siglecs.Molecular aspects of medicine · 2023Review
- Identification of cerebral spinal fluid protein biomarkers in Niemann-Pick disease, type C1.Biomarker research · 2023Article
- Leveraging iPSC technology to assess neuro-immune interactions in neurological and psychiatric disorders.Frontiers in psychiatry · 2023Review
- High-Throughput Analysis Reveals miRNA Upregulating α-2,6-Sialic Acid through Direct miRNA-mRNA Interactions.ACS central science · 2022Article
- Recent Advances in Microglia Modelling to Address Translational Outcomes in Neurodegenerative Diseases.Cells · 2022Review
- Associations of plasma soluble CD22 levels with brain amyloid burden and cognitive decline in Alzheimer's disease.Science advances · 2022Article
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Authors and funding
22 authors.
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Abstract
Lysosome dysfunction is a shared feature of rare lysosomal storage diseases and common age-related neurodegenerative diseases. Microglia, the brain-resident macrophages, are particularly vulnerable to lysosome dysfunction because of the phagocytic stress of clearing dying neurons, myelin, and debris. CD22 is a negative regulator of microglial homeostasis in the aging mouse brain, and soluble CD22 (sCD22) is increased in the cerebrospinal fluid of patients with Niemann-Pick type C disease (NPC). However, the role of CD22 in the human brain remains unknown. In contrast to previous findings in mice, here, we show that CD22 is expressed by oligodendrocytes in the human brain and binds to sialic acid–dependent ligands on microglia. Using unbiased genetic and proteomic screens, we identify insulin-like growth factor 2 receptor (IGF2R) as the binding partner of sCD22 on human myeloid cells. Targeted truncation of IGF2R revealed that sCD22 docks near critical mannose 6-phosphate–binding domains, where it disrupts lysosomal protein trafficking. Interfering with the sCD22-IGF2R interaction using CD22 blocking antibodies ameliorated lysosome dysfunction in human
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