Evidence map›Paper›PMID 36012120›Full record

ArticleInternational journal of molecular sciences2022

Inhibition of TREM-2 Markedly Suppresses Joint Inflammation and Damage in Experimental Arthritis.

Alexander B Sigalov

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. TREM2-Targeting peptide tracer for neuroinflammation PET imaging.European journal of nuclear medicine and molecular imaging · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Nanoparticle Delivery Systems in Rheumatoid Arthritis: More Than Vehicles.Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Review
  8. TREM2-driven peripheral macrophage regulation in inflammatory diseases: implications extending beyond neurological disorders.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Research of Pathogenesis and Novel Therapeutics in Arthritis 3.0.International journal of molecular sciences · 2023
    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

1 author at 1 institution in 1 country.

Alexander B SigalovSignaBlok, Inc., P.O. Box 4064, Shrewsbury, MA 01545, USA.
SignaBlok (United States) · US

Funding

TREM-1 therapy for rheumatoid arthritisR44AR077456 · NIAMS · SIGNABLOK, INC. · PI SIGALOV, ALEXANDER B · 2020 to 2020
$259k
National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health R44AR077456NIAMS NIH HHS R44 AR077456
6 · The paper itself

Abstract

The triggering receptors expressed on myeloid cells (TREMs) are a family of activating immune receptors that regulate the inflammatory response. TREM-1, which is expressed on monocytes and/or macrophages and neutrophils, functions as an inflammation amplifier and plays a role in the pathogenesis of rheumatoid arthritis (RA). Unlike TREM-1, the role in RA of TREM-2, which is expressed on macrophages, immature monocyte-derived dendritic cells, osteoclasts, and microglia, remains unclear and controversial. TREM-2 ligands are still unknown, adding further uncertainty to our understanding of TREM-2 function. Previously, we demonstrated that TREM-1 blockade, using a ligand-independent TREM-1 inhibitory peptide sequence GF9 rationally designed by our signaling chain homooligomerization (SCHOOL) model of cell signaling, ameliorates collagen-induced arthritis (CIA) severity in mice. Here, we designed a TREM-2 inhibitory peptide sequence IA9 and tested it in the therapeutic CIA model, either as a free 9-mer peptide IA9, or as a part of a 31-mer peptide IA31 incorporated into lipopeptide complexes (IA31-LPC), for targeted delivery. We demonstrated that administration of IA9, but not a control peptide, after induction of arthritis diminished release of proinflammatory cytokines and dramatically suppressed joint inflammation and damage, suggesting that targeting TREM-2 may be a promising approach for the treatment of RA.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidAnimalsInflammationMembrane GlycoproteinsMicePeptidesReceptors, ImmunologicTriggering Receptor Expressed on Myeloid Cells-1Membrane GlycoproteinsPeptidesReceptors, ImmunologicTrem2 protein, mouseTriggering Receptor Expressed on Myeloid Cells-1cytokinesdrug delivery systemsinflammationinnate immunitymacrophagesnanomedicinerheumatoid arthritissignal transductionTREM-1TREM-2triggering receptors expressed on myeloid cells

Identifiers

PMID36012120
PMCPMC9408405
OpenAlexW4293511048

What OpenQuestion holds

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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.