ArticleFrontiers in immunology2024
IgG sialylation occurs in B cells pre antibody secretion.
Article in Frontiers in immunology, 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.
- B cell mechanisms underlie IgG glycan alterations in obesity.Glycobiology · 2026Article
- Interleukin-10 enhances IgG galactosylation and sialylation.Biomarker research · 2026Article
- Systemic Inflammation as a Modulator of FcRn-dependent IgG Pharmacokinetics: Implications for Broadly Neutralising Antibody Efficacy in HIV Prevention.Current HIV/AIDS reports · 2026Review
- Endothelial cells sialylate IgG within the FcRn-mediated recycling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Splenic comparative transcriptome analysis reveals the immunological mode of undomesticated Gayal (Bos frontalis) for adapting to harsh environments.BMC genomics · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sialic acids as terminal sugar residues on cell surface or secreted proteins have many functional roles. In particular, the presence or absence of α2,6-linked sialic acid residues at the immunoglobulin G (IgG) Fc fragment can switch IgG effector functions from pro- to anti-inflammatory activity. IgG glycosylation is considered to take place inside the plasma blast/plasma cell while the molecule travels through the endoplasmic reticulum and Golgi apparatus before being secreted. However, more recent studies have suggested that IgG sialylation may occur predominantly post-antibody secretion. To what extent this extracellular IgG sialylation process contributes to overall IgG sialylation remains unclear, however. By generating bone marrow chimeric mice with a B cell-specific deletion of ST6Gal1, the key enzyme required for IgG sialylation, we now show that sialylation of the IgG Fc fragment exclusively occurs within B cells pre-IgG secretion. We further demonstrate that B cells expressing ST6Gal1 have a developmental advantage over B cells lacking ST6Gal1 expression and thus dominate the plasma cell pool and the resulting serum IgG population in mouse models in which both ST6Gal1-sufficient and -deficient B cells are present.
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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 Socratic graph.