ArticleSelf/nonself2010
Triggering receptor expressed on myeloid cells-1 as a new therapeutic target during inflammatory diseases.
Article in Self/nonself, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed, 40 citations in OpenAlex.
- Nangibotide in patients with septic shock: a Phase 2a randomized controlled clinical trial.Intensive care medicine · 2020Trial
- A first-in-man safety and pharmacokinetics study of nangibotide, a new modulator of innate immune response through TREM-1 receptor inhibition.British journal of clinical pharmacology · 2018Trial
- As48, a first-in-class dual-function TREM2 modulator: Receptor activation and shedding inhibition.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- N6-methyladenosine-mediated overexpression of TREM-1 is associated with periodontal disease.Odontology · 2025Article
- Article
- Serum Levels of Soluble Triggering Receptor Expressed on Myeloid Cells-1 Associated with the Severity and Outcome of Acute Ischemic Stroke.Journal of clinical medicine · 2020Article
- Review
- TREM-1; Is It a Pivotal Target for Cardiovascular Diseases?Journal of cardiovascular development and disease · 2018Review
- Tumor necrosis factor-α regulates triggering receptor expressed on myeloid cells-1-dependent matrix metalloproteinases in the carotid plaques of symptomatic patients with carotid stenosis.Atherosclerosis · 2016Article
- Toll-like receptors, triggering receptor expressed on myeloid cells family members and receptor for advanced glycation end-products in allergic airway inflammation.Expert review of respiratory medicine · 2016Review
- Inactivation of DAP12 in PMN inhibits TREM1-mediated activation in rheumatoid arthritis.PloS one · 2015Article
- Multigene families of immunoglobulin domain-containing innate immune receptors in zebrafish: deciphering the differences.Developmental and comparative immunology · 2014Review
- TREM-1 as a potential therapeutic target in neonatal sepsis.International journal of clinical and experimental medicine · 2014Article
- TLR-2/TLR-4 TREM-1 signaling pathway is dispensable in inflammatory myeloid cells during sterile kidney injury.PloS one · 2013Article
- The immunopathology of sepsis: pathogen recognition, systemic inflammation, the compensatory anti-inflammatory response, and regulatory T cells.Journal of veterinary internal medicineReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Triggering Receptor Expressed on Myeloid cells (TREM)-1 is a recently identified molecule involved in monocytic activation and inflammatory response. It belongs to a family related to Natural Killer cell-receptors and is expressed on neutrophils, mature monocytes and macrophages. The engagement of TREM-1 synergizes with several Toll Like Receptors (TLR) and/or NOD Like Receptors (NLR) activation in amplifying the inflammatory response mediated by microbial components or danger signals. The implication of TREM-1 during experimental models of acute or chronic inflammatory conditions, as well as during cancer, begins to understand. Furthermore, the modulation of the TREM-1 signaling pathway by the use of small synthetic peptides derived from its extracellular moiety confers interesting survival advantages during experimental murine septic shock and protects from organ damage during other inflammatory diseases. This review summarizes the recent advances on TREM-1 biology and highlights the promises of its therapeutic modulation.
Identifiers
What OpenQuestion holds
Registered trials
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.