Evidence map›Paper›PMID 26106150›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

DC-SIGN activation mediates the differential effects of SAP and CRP on the innate immune system and inhibits fibrosis in mice.

Nehemiah Cox, Darrell Pilling, Richard H Gomer

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Inhibiting Sialidase-Induced TGF-The Journal of pharmacology and experimental therapeutics · 2021
    Article
  16. Article
  17. Article
  18. Attenuated pulmonary fibrosis in sialidase-3 knockout (American journal of physiology. Lung cellular and molecular physiology · 2020
    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

3 authors at 1 institution in 1 country.

Nehemiah CoxDepartment of Biology, MS-3474, Texas A&M University, College Station, TX 77843-3474.
Darrell PillingDepartment of Biology, MS-3474, Texas A&M University, College Station, TX 77843-3474.
Richard H GomerDepartment of Biology, MS-3474, Texas A&M University, College Station, TX 77843-3474 rgomer@tamu.edu.
Texas A&M University · US

Funding

Pentraxin regulation of macrophage differentiationR01HL118507 · NHLBI · TEXAS A&M UNIVERSITY · PI GOMER, RICHARD H · 2014 to 2017
$1.4M
NHLBI NIH HHS R01 HL118507
6 · The paper itself

Abstract

Fibrosis is caused by scar tissue formation in internal organs and is associated with 45% of deaths in the United States. Two closely related human serum proteins, serum amyloid P (SAP) and C-reactive protein (CRP), strongly affect fibrosis. In multiple animal models, and in Phase 1 and Phase 2 clinical trials, SAP affects several aspects of the innate immune system to reduce fibrosis, whereas CRP appears to potentiate fibrosis. However, SAP and CRP bind the same Fcγ receptors (FcγR) with similar affinities, and why SAP and CRP have opposing effects is unknown. Here, we report that SAP but not CRP binds the receptor DC-SIGN (SIGN-R1) to affect the innate immune system, and that FcγR are not necessary for SAP function. A polycyclic aminothiazole DC-SIGN ligand and anti-DC-SIGN antibodies mimic SAP effects in vitro. In mice, the aminothiazole reduces neutrophil accumulation in a model of acute lung inflammation and, at 0.001 mg/kg, alleviates pulmonary fibrosis by increasing levels of the immunosuppressant IL-10. DC-SIGN (SIGN-R1) is present on mouse lung epithelial cells, and SAP and the aminothiazole potentiate IL-10 production from these cells. Our data suggest that SAP activates DC-SIGN to regulate the innate immune system differently from CRP, and that DC-SIGN is a target for antifibrotics.

Indexed as

AnimalsBlotting, WesternCell Adhesion MoleculesCells, CulturedC-Reactive ProteinDC-Specific ICAM-3 Grabbing NonintegrinHEK293 CellsHumansImmunity, InnateInterleukin-10Lectins, C-TypeLungMacrophagesMice, Inbred C57BLMice, KnockoutMicroscopy, Confocal2-aminothiazoleCell Adhesion MoleculesC-Reactive ProteinDC-Specific ICAM-3 Grabbing NonintegrinInterleukin-10Lectins, C-TypeReceptors, Cell SurfaceReceptors, IgGSerum Amyloid P-ComponentThiazolesDC-SIGNfibrosisIL-10pentraxinserum amyloid P

Identifiers

PMID26106150
PMCPMC4500200
OpenAlexW1536248267

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.