Evidence map›Paper›PMID 32745987›Full record

ArticleiScience2020

N-Glycan Branching Decouples B Cell Innate and Adaptive Immunity to Control Inflammatory Demyelination.

Christie-Lynn Mortales, Sung-Uk Lee, Armen Manousadjian, Ken L Hayama, Michael Demetriou

Open access · goldAbstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. PlasmaNeurology(R) neuroimmunology & neuroinflammation · 2025
    Article
  4. Improvement of Spontaneous Locomotor Activity in a Murine Model of Duchenne Muscular Dystrophy by N-Acetylglucosamine Alone and in Combination With Prednisolone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Deletion ofFrontiers in cell and developmental biology · 2024
    Article
  11. The role of glycosylation in clinical allergy and immunology.The Journal of allergy and clinical immunology · 2024
    Review
  12. Review
  13. Immunometabolism (Cobham, Surrey) · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Christie-Lynn MortalesDepartment of Microbiology & Molecular Genetics, University of California, Irvine, CA 92617, USA.
Sung-Uk LeeDepartment of Neurology, University of California, Irvine, CA 92617, USA.
Armen ManousadjianDepartment of Neurology, University of California, Irvine, CA 92617, USA.
Ken L HayamaDepartment of Microbiology & Molecular Genetics, University of California, Irvine, CA 92617, USA.
Michael DemetriouDepartment of Neurology, University of California, Irvine, CA 92617, USA; Department of Microbiology & Molecular Genetics, University of California, Irvine, CA 92617, USA. Electronic address: mdemetri@uci.edu.
University of California, Irvine · US

Funding

Regulation of B cell function in demyelinating disease by N-glycan branchingR01AI144403 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI DEMETRIOU, MICHAEL · 2019 to 2023
$2.5M
Immunology Research Training ProgramT32AI060573 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI PEARLMAN, ERIC · 2005 to 2020
$1.9M
NIAID NIH HHS R01 AI144403NIAID NIH HHS T32 AI060573
6 · The paper itself

Abstract

B cell depletion potently reduces episodes of inflammatory demyelination in multiple sclerosis (MS), predominantly through loss of innate rather than adaptive immunity. However, molecular mechanisms controlling innate versus adaptive B cell function are poorly understood. N-glycan branching, via interactions with galectins, controls endocytosis and signaling of cell surface receptors to control cell function. Here we report that N-glycan branching in B cells dose dependently reduces pro-inflammatory innate responses by titrating decreases in Toll-like receptor-4 (TLR4) and TLR2 surface expression via endocytosis. In contrast, a minimal level of N-glycan branching maximizes surface retention of the B cell receptor (BCR) and the CD19 co-receptor to promote adaptive immunity. Branched N-glycans inhibit antigen presentation by B cells to reduce T helper cell-17 (T

Indexed as

ImmunologyMolecular BiologyNeuroscience

Identifiers

PMID32745987
PMCPMC7398982
OpenAlexW3043422039

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.