ArticleThe Journal of experimental medicine2009
Group B Streptococcus suppression of phagocyte functions by protein-mediated engagement of human Siglec-5.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
102 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.
- Genome-wide association meta-analysis identifies two novel loci associated with dental caries.BMC oral health · 2024Pooled it
- Bacterial targeting of the neutrophil inhibitory receptor LILRB3 to evade antibody immunity.Nature communications · 2026Article
- Flagellar glycosylation with pseudaminic acids is widespread in the genus Clostridium.BMC microbiology · 2026Article
- Mitochondria as Inducers of Neutrophil Extracellular Traps.Inflammation · 2026Review
- Unravelling mechanisms regulating Mincle activation.Communications biology · 2026Review
- Global genome analysis identifies glycolipids and lipoteichoic acid alanylation as contributors to group B streptococcal diabetic wound infection.Cell reports · 2025Article
- Identification of glyoxalase A in group BInfection and immunity · 2025Article
- Biochemical and biophysical mechanisms macrophages use to tune phagocytic appetite.Journal of cell science · 2025Review
- Cell death in acute lung injury: caspase-regulated apoptosis, pyroptosis, necroptosis, and PANoptosis.Frontiers in pharmacology · 2025Review
- Identification of Glyoxalase A in Group BbioRxiv : the preprint server for biology · 2024Article
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- Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota.Nature communications · 2024Article
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- Insights into the recognition of hypermucoviscousFrontiers in immunology · 2024Article
- Strain-level genomic analysis of serotype, genotype and virulence gene composition of group B streptococcus.Frontiers in cellular and infection microbiology · 2024Article
- An inflammatory paradox: strategies inflammophilic oral pathobionts employ to exploit innate immunity via neutrophil manipulation.Frontiers in oral health · 2024Article
- Neutrophil extracellular traps in bacterial infections and evasion strategies.Frontiers in immunology · 2024Review
- Comparative physiological anthropogeny: exploring molecular underpinnings of distinctly human phenotypes.Physiological reviews · 2023Review
- Recent progress in targeting the sialylated glycan-SIGLEC axis in cancer immunotherapy.Cancer biology & medicine · 2023Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
Group B Streptococcus (GBS) is a leading cause of invasive bacterial infections in human newborns. A key GBS virulence factor is its capsular polysaccharide (CPS), displaying terminal sialic acid (Sia) residues which block deposition and activation of complement on the bacterial surface. We recently demonstrated that GBS Sia can bind human CD33-related Sia-recognizing immunoglobulin (Ig) superfamily lectins (hCD33rSiglecs), a family of inhibitory receptors expressed on the surface of leukocytes. We report the unexpected discovery that certain GBS strains may bind one such receptor, hSiglec-5, in a Sia-independent manner, via the cell wall-anchored beta protein, resulting in recruitment of SHP protein tyrosine phosphatases. Using a panel of WT and mutant GBS strains together with Siglec-expressing cells and soluble Siglec-Fc chimeras, we show that GBS beta protein binding to Siglec-5 functions to impair human leukocyte phagocytosis, oxidative burst, and extracellular trap production, promoting bacterial survival. We conclude that protein-mediated functional engagement of an inhibitory host lectin receptor promotes bacterial innate immune evasion.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.