Evidence map›Paper›PMID 36055802›Full record

ReviewMolecular aspects of medicine2023

Impact of Siglecs on autoimmune diseases.

Katarzyna Alicja Brzezicka, James C Paulson

Open access · greenAbstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Diagnostic significance of salivary and glandular siglec-5 in Sjögren disease and non-Sjögren sicca.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Siglecs: From Biomodulation to Immunotherapy.Current protein & peptide science · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. 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

2 authors at 1 institution in 1 country.

Katarzyna Alicja BrzezickaDepartment of Molecular Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, 92037, USA; Department of Immunology and Microbiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, 92037, USA.
James C PaulsonDepartment of Molecular Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, 92037, USA; Department of Immunology and Microbiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, 92037, USA. Electronic address: jpaulson@scripps.edu.
Scripps Research Institute · US

Funding

REGULATION OF SIALOSIDE EXPRESSION IN LEUKOCYTESR01AI050143 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI PAULSON, JAMES C · 2003 to 2018
$7.0M
Exploiting inhibitory Siglecs for desensitizing mast cellsR01AI132790 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI PAULSON, JAMES C · 2018 to 2022
$3.1M
NIAID NIH HHS R01 AI050143NIAID NIH HHS R01 AI132790
6 · The paper itself

Abstract

Autoimmune diseases affect tens of millions of people just in the United States alone. Most of the available treatment options are aimed at reducing symptoms but do not lead to cures. Individuals affected with autoimmune diseases suffer from the imbalance between tolerogenic and immunogenic functions of their immune system. Often pathogenesis is mediated by autoreactive B and T cells that escape central tolerance and react against self-antigens attacking healthy tissues in the body. In recent years Siglecs, sialic-acid-binding immunoglobulin (Ig)-like lectins, have gained attention as immune checkpoints for therapeutic interventions to dampen excessive immune responses and to restore immune tolerance in autoimmune diseases. Many Siglecs function as inhibitory receptors suppressing activation signals in various immune cells through binding to sialic acid ligands as signatures of self. In this review, we highlight potential of Siglecs in suppressing immune responses causing autoimmune diseases. In particular, we cover the roles of CD22 and Siglec-G/Siglec-10 in regulating autoreactive B cell responses. We discuss several functions of Siglec-10 in the immune modulation of other immune cells, and the potential of therapeutic strategies for restoring immune tolerance by targeting Siglecs and expanding regulatory T cells. Finally, we briefly review efforts evaluating Siglec-based biomarkers to monitor autoimmune diseases.

Indexed as

Autoimmune DiseasesSialic Acid Binding Immunoglobulin-like LectinsB-LymphocytesHumansN-Acetylneuraminic AcidSialic Acid Binding Ig-like Lectin 2N-Acetylneuraminic AcidSialic Acid Binding Ig-like Lectin 2Sialic Acid Binding Immunoglobulin-like LectinsAutoimmune diseasesAutoreactive B cellsRegulatory T cellsSiglec-1Siglec-2Siglec-G/10

Identifiers

PMID36055802
PMCPMC9905255
OpenAlexW4293558178

What OpenQuestion holds

Textmetadata
LicenceTDM
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.