Evidence map›Paper›PMID 25247291›Full record

ArticleMolecular medicine (Cambridge, Mass.)2015

C1q-mediated repression of human monocytes is regulated by leukocyte-associated Ig-like receptor 1 (LAIR-1).

Myoungsun Son, Betty Diamond

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. The frequency of CD38Nature communications · 2024
    Article
  6. Article
  7. Article
  8. LAIR-1 agonism as a therapy for acute myeloid leukemia.The Journal of clinical investigation · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Type I Interferon Production of Plasmacytoid Dendritic Cells under Control.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Myoungsun SonCenter for Autoimmune and Musculoskeletal Diseases, Feinstein Institute for Medical Research, Manhasset, New York, United States of America.
Betty DiamondCenter for Autoimmune and Musculoskeletal Diseases, Feinstein Institute for Medical Research, Manhasset, New York, United States of America.
Feinstein Institute for Medical Research · US

Funding

Antibodies to NR2 in SLER01AR049126 · NIAMS · YESHIVA UNIVERSITY · PI DIAMOND, BETTY · 2002 to 2011
$3.8M
Toward a new approach to SLE therapyR01AR057084 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DIAMOND, BETTY · 2010 to 2014
$1.8M
Regulation of LAIR-1 in LupusK01AR065506 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SON, MYOUNGSUN · 2014 to 2018
$639k
NIAMS NIH HHS K01 AR065506NIAMS NIH HHS R01 AR049126NIAMS NIH HHS R01AR-049126
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by abnormal function of both the innate and the adaptive immune system, leading to a loss of tolerance to self-antigens. Monocytes are a key component of the innate immune system and are efficient producers of multiple cytokines. In SLE, inappropriate activation of monocytes is thought to contribute to the loss of self-tolerance. In this study, we demonstrate that type 1 interferon (IFN) production by CpG-challenged monocytes can be suppressed by C1q through activating leukocyte-associated Ig-like receptor-1 (LAIR-1), which contains immunoreceptor tyrosine-based inhibition motifs (ITIMs). The phosphorylation of LAIR-1 and the interaction of LAIR-1 with SH2 domain-containing protein tyrosine phosphatase-1 (SHP-1) were enhanced after LAIR-1 engagement by C1q. Moreover, engagement of LAIR-1 by C1q inhibited nuclear translocation of interferon regulatory factor (IRF)-3 and IRF5 in CpG-stimulated monocytes. These data suggest a model in which LAIR-1 engagement by C1q helps maintain monocyte tolerance, specifically with respect to Toll-like receptor-9-mediated monocyte activation.

Indexed as

Cells, CulturedComplement C1qCpG IslandsGene Expression RegulationHumansInterferon-gammaInterleukin-6MonocytesProtein Tyrosine Phosphatase, Non-Receptor Type 6Receptors, ImmunologicRNA, Small InterferingTumor Necrosis Factor-alphaComplement C1qIL6 protein, humanInterferon-gammaInterleukin-6leukocyte-associated immunoglobulin-like receptor 1Protein Tyrosine Phosphatase, Non-Receptor Type 6PTPN6 protein, humanReceptors, ImmunologicRNA, Small InterferingTumor Necrosis Factor-alpha

Identifiers

PMID25247291
PMCPMC4365071
OpenAlexW959290310

What OpenQuestion holds

Textmetadata
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.