ArticleProceedings of the National Academy of Sciences of the United States of America2018
CD52 glycan binds the proinflammatory B box of HMGB1 to engage the Siglec-10 receptor and suppress human T cell function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 84 citations in OpenAlex.
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- Integrated scRNA-Seq and functional profiling reveal CD52 as a driver of pancreatic ductal adenocarcinoma metastasis and immunosuppression.Oncogenesis · 2026Article
- An atlas of human siglecs integrates expression, affinity, and cis/trans sialoglycan recognition profiles.Nature communications · 2026Article
- ScRNA-Seq and BCR Analysis of Murine Immune Responses to Inactivated DHAV-1 as a Model Antigen.Viruses · 2026Article
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- A synergistic multi-omics approach: causal sepsis drivers identified in activated CD4Frontiers in cellular and infection microbiology · 2026Article
- MYD88 regulates the intercellular crosstalk landscape in MASH liver against metaflammation and metabolic disorder.Acta pharmaceutica Sinica. B · 2025Article
- DNA methylation-mediated ADA overexpression drives pancreatic cancer progression.Discover oncology · 2025Article
- Discovery and characterization of vertebrate sialoglycan-binding proteins.Seminars in immunology · 2025Review
- Differential susceptibility and role for senescence in CART cells based on costimulatory domains.Molecular cancer · 2025Article
- Exploring Glycan-Lectin Interactions in Natural-Like Environments: A View Using NMR Experiments Inside Cell and on Cell Surface.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025Article
- EDF1 accelerates ganglioside GD3 accumulation to boost CD52-mediated CD8Journal of experimental & clinical cancer research : CR · 2025Article
- Sidedness matters: single-cell perspectives on left- and right-sided colorectal cancer.Frontiers in cell and developmental biology · 2025Review
- Identification of novel prognostic biomarkers for thyroid cancer by integrated transcriptome analysis of metastasis-associated genes.Frontiers in oncology · 2025Article
- Genome-wide transcriptome analysis and drug target discovery reveal key genes and pathways in thyroid cancer metastasis.Frontiers in endocrinology · 2025Article
- Siglec-G Suppresses CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Wilson's Disease-Crossroads of Genetics, Inflammation and Immunity/Autoimmunity: Clinical and Molecular Issues.International journal of molecular sciences · 2024Review
- Distinct fibroblast subpopulations associated with bone, brain or intrapulmonary metastasis in advanced non-small-cell lung cancer.Clinical and translational medicine · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD52, a glycophosphatidylinositol (GPI)-anchored glycoprotein, is released in a soluble form following T cell activation and binds to the Siglec (sialic acid-binding Ig-like lectin)-10 receptor on T cells to suppress their function. We show that binding of CD52-Fc to Siglec-10 and T cell suppression requires the damage-associated molecular pattern (DAMP) protein, high-mobility group box 1 (HMGB1). CD52-Fc bound specifically to the proinflammatory Box B domain of HMGB1, and this in turn promoted binding of the CD52 N-linked glycan, in α-2,3 sialic acid linkage with galactose, to Siglec-10. Suppression of T cell function was blocked by anti-HMGB1 antibody or the antiinflammatory Box A domain of HMGB1. CD52-Fc induced tyrosine phosphorylation of Siglec-10 and was recovered from T cells complexed with HMGB1 and Siglec-10 in association with SHP1 phosphatase and the T cell receptor (TCR). Thus, soluble CD52 exerts a concerted immunosuppressive effect by first sequestering HMGB1 to nullify its proinflammatory Box B, followed by binding to the inhibitory Siglec-10 receptor, triggering recruitment of SHP1 to the intracellular immunoreceptor tyrosine-based inhibitory motif of Siglec-10 and its interaction with the TCR. This mechanism may contribute to immune-inflammatory homeostasis in pathophysiologic states and underscores the potential of soluble CD52 as a therapeutic agent.
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