Evidence map›Paper›PMID 30559744›Full record

ReviewFrontiers in immunology2018

B Cell Siglecs-News on Signaling and Its Interplay With Ligand Binding.

Sarah J Meyer, Alexandra T Linder, Carolin Brandl, Lars Nitschke

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Impact of Siglecs on autoimmune diseases.Molecular aspects of medicine · 2023
    Review
  13. Glycobiology of rheumatic diseases.Nature reviews. Rheumatology · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Sialic acids on B cells are crucial for their survival and provide protection against apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Article
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Sarah J MeyerDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Alexandra T LinderDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Carolin BrandlDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Lars NitschkeDivision of Genetics, Department of Biology, University of Erlangen, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD22 and Siglec-G are members of the Siglec family. Both are inhibitory co-receptors on the surface of B cells and inhibit B-cell receptor induced signaling, characterized by inhibition of the calcium mobilization and cellular activation. CD22 functions predominantly as an inhibitor on conventional B cells, while Siglec-G is an important inhibitor on the B1a-cell subset. These two B-cell Siglecs do not only inhibit initial signaling, but also have an important function in preventing autoimmunity, as double deficient mice develop a lupus-like phenotype with age. Siglecs are characterized by their conserved ability to bind terminal sialic acid of glycans on the cell surface, which is important to regulate the inhibitory role of Siglecs. While CD22 binds α2,6-linked sialic acids, Siglec-G can bind both α2,6-linked and α2,3-linked sialic acids. Interestingly, ligand binding is differentially regulating the ability of CD22 and Siglec-G to control B-cell activation. Within the last years, quite a few studies focused on the different functions of B-cell Siglecs and the interplay of ligand binding and signal inhibition. This review summarizes the role of CD22 and Siglec-G in regulating B-cell receptor signaling, membrane distribution with the importance of ligand binding, preventing autoimmunity and the role of CD22 beyond the naïve B-cell stage. Additionally, this review article features the long time discussed interaction between CD45 and CD22 with highlighting recent data, as well as the interplay between CD22 and Galectin-9 and its influence on B-cell receptor signaling. Moreover, therapeutical approaches targeting human CD22 will be elucidated.

Indexed as

AnimalsAutoimmunityB-LymphocytesGalectinsHumansLeukocyte Common AntigensLigandsN-Acetylneuraminic AcidPolysaccharidesReceptors, Antigen, B-CellSialic Acid Binding Ig-like Lectin 2Sialic Acid Binding Immunoglobulin-like LectinsSignal TransductionGalectinsLeukocyte Common AntigensLigandsN-Acetylneuraminic AcidPolysaccharidesReceptors, Antigen, B-CellSialic Acid Binding Ig-like Lectin 2Sialic Acid Binding Immunoglobulin-like LectinsB lymphocytesCD22inhibitory receptorssialic acidSiglec

Identifiers

PMID30559744
PMCPMC6286995
OpenAlexW2903237949

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.