Evidence map›Paper›PMID 23720814›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Endogenous galectin-1 exerts tonic inhibition on experimental arthritis.

Asif J Iqbal, Dianne Cooper, Alexander Vugler, Beatrice R Gittens, Adrian Moore, Mauro Perretti

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Suppression of age-related salivary gland autoimmunity by glycosylation-dependent galectin-1-driven immune inhibitory circuits.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Anti-inflammatory effect of galectin-1 in a murine model of atopic dermatitis.Journal of molecular medicine (Berlin, Germany) · 2017
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Galectins in the Pathogenesis of Rheumatoid Arthritis.Journal of clinical & cellular immunology · 2013
    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

6 authors at 2 institutions in 1 country.

Asif J IqbalWilliam Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London, London, United Kingdom.
Dianne Cooper
Alexander Vugler
Beatrice R Gittens
Adrian Moore
Mauro Perretti
William Harvey Research Institute · GBUCB Pharma (United Kingdom) · GB

Funding

Arthritis Research UK 18103Biotechnology and Biological Sciences Research CouncilVersus Arthritis 18103
6 · The paper itself

Abstract

Little is known about the role(s) of endogenous galectin-1 (Gal-1) in arthritis. In this study we queried whether antiarthritic functions for this effector of endogenous anti-inflammation could be unveiled by studying collagen-induced arthritis in Gal-1(-/-) mice. Gal-1(-/-) and C57BL/6J [wild-type (WT)] mice received an immunization of chicken type II collagen (CII) in CFA followed by a booster on day 21, which consisted of CII in IFA. Animals were monitored for signs of arthritis from day 14 onward. Clinical and histological signs of arthritis were recorded, and humoral and cellular immune responses against CII were analyzed. A distinct disease penetrance was apparent, with ~ 70% of Gal-1(-/-) mice developing arthritis compared with ~ 50% in WT animals. Gal-1(-/-) mice also exhibited an accelerated disease onset and more severe arthritis characterized by significantly elevated clinical scores. Postmortem analyses (day 42) revealed higher levels of IgG1 and IgG2b anti-CII Ig isotypes in the serum of Gal-1 null animals compared with WT. Finally, T cell responses following ex vivo stimulation with CII revealed a greater degree of proliferation in T cells of Gal-1(-/-) mice compared with WT, which was associated with increased production of IL-17 and IL-22. These data suggest the novel idea that endogenous Gal-1 is an inhibitory factor in the development of arthritis affecting disease severity. We have also highlighted the importance of endogenous Gal-1 in regulating T cell reactivity during experimental arthritis.

Indexed as

AnimalsArthritis, ExperimentalFemaleGalectin 1Gene Expression RegulationIncidenceMaleMiceMice, Inbred C57BLMice, Inbred DBAMice, KnockoutSeverity of Illness IndexGalectin 1

Identifiers

PMID23720814
PMCPMC3971374
OpenAlexW2132166259

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.