Evidence map›Paper›PMID 27083877›Full record

ArticleInflammation2016

Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis.

Yong Du, Tianfu Wu, Xin J Zhou, Laurie S Davis, Chandra Mohan

Open access · hybridAbstract read
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The biology of TREM receptors.Nature reviews. Immunology · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. TREM-1 Contributes to Inflammation in IgA Nephropathy.Kidney diseases (Basel, Switzerland) · 2018
    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

5 authors at 1 institution in 1 country.

Yong DuDivision of Rheumatology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Bldg Y, Flr 8, Room 206 (Y8.206), Dallas, TX, 75390-8884, USA.
Tianfu WuDivision of Rheumatology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Bldg Y, Flr 8, Room 206 (Y8.206), Dallas, TX, 75390-8884, USA.
Xin J ZhouDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Laurie S DavisDivision of Rheumatology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Bldg Y, Flr 8, Room 206 (Y8.206), Dallas, TX, 75390-8884, USA. Laurie.Davis@UTSouthwestern.edu.
Chandra MohanDivision of Rheumatology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Bldg Y, Flr 8, Room 206 (Y8.206), Dallas, TX, 75390-8884, USA.
The University of Texas Southwestern Medical Center · US

Funding

SLAM Genes-from Mouse to ManP50AR055503 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI KARP, DAVID R · 2007 to 2011
$8.3M
Foreboding Lupus Nephritis in Minority WomanR01DK081872 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOHAN, CHANDRA · 2009 to 2013
$2.4M
NIAMS NIH HHS P50 AR055503NIDDK NIH HHS R01 DK081872
6 · The paper itself

Abstract

CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis.

Indexed as

AnimalsAutoantibodiesDisease Models, AnimalLupus NephritisMembrane GlycoproteinsMiceMice, Inbred StrainsRabbitsReceptors, ImmunologicRNA, MessengerTriggering Receptor Expressed on Myeloid Cells-1Up-Regulationantiglomerular basement membrane antibodyAutoantibodiesMembrane GlycoproteinsReceptors, ImmunologicRNA, MessengerTREM1 protein, mouseTriggering Receptor Expressed on Myeloid Cells-1anti-glomerular basement membrane antibody-induced nephritisimmune-mediated nephritisimmunotherapySLE, systemic lupus erythematosusTriggering Receptor Expressed by Myeloid Cells-1 (TREM-1)

Identifiers

PMID27083877
PMCPMC4883274
OpenAlexW2336902892

What OpenQuestion holds

Textmetadata
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.