Evidence map›Paper›PMID 28619036›Full record

ArticleBMC immunology2017

Monocyte differentiation and macrophage priming are regulated differentially by pentraxins and their ligands.

Darrell Pilling, Elkin Galvis-Carvajal, Tejas R Karhadkar, Nehemiah Cox, Richard H Gomer

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  4. Advances in idiopathic pulmonary fibrosis diagnosis and treatment.Chinese medical journal pulmonary and critical care medicine · 2025
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  8. Macrophage variants in laboratory research: most are well done, but some are RAW.Frontiers in cellular and infection microbiology · 2024
    Review
  9. Review
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  13. Review
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  15. Idiopathic pulmonary fibrosis: Current and future treatment.The clinical respiratory journal · 2022
    Review
  16. Article
  17. Article
  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

5 authors at 1 institution in 1 country.

Darrell PillingDepartment of Biology, Texas A&M University, 3474 TAMU, College Station, TX, 77843-3474, USA. dpilling@bio.tamu.edu.ORCID 0000-0002-7413-2773
Elkin Galvis-CarvajalDepartment of Biology, Texas A&M University, 3474 TAMU, College Station, TX, 77843-3474, USA.
Tejas R KarhadkarDepartment of Biology, Texas A&M University, 3474 TAMU, College Station, TX, 77843-3474, USA.
Nehemiah CoxDepartment of Biology, Texas A&M University, 3474 TAMU, College Station, TX, 77843-3474, USA.
Richard H GomerDepartment of Biology, Texas A&M University, 3474 TAMU, College Station, TX, 77843-3474, USA.
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

backgroundCirculating bone marrow-derived monocytes can leave the blood, enter a tissue, and differentiate into M1 inflammatory, M2a remodeling/fibrotic, or M2c/Mreg resolving/immune-regulatory macrophages. Macrophages can also convert from one of the above types to another. Pentraxins are secreted proteins that bind to, and promote efficient clearance of, microbial pathogens and cellular debris during infection, inflammation, and tissue damage. The pentraxins C-reactive protein (CRP), serum amyloid P (SAP), and pentraxin-3 (PTX3) can also bind a variety of endogenous ligands. As monocytes and macrophages are exposed to differing concentrations of pentraxins and their ligands during infection, inflammation, and tissue damage, we assessed what effect pentraxins and their ligands have on these cells.

resultsWe found that many polarization markers do not discriminate between the effects of pentraxins and their ligands on macrophages. However, pentraxins, their ligands, and cytokines differentially regulate the expression of the hemoglobin-haptoglobin complex receptor CD163, the sialic acid-binding lectin CD169, and the macrophage mannose receptor CD206. CRP, a pentraxin generally thought of as being pro-inflammatory, increases the extracellular accumulation of the anti-inflammatory cytokine IL-10, and this effect is attenuated by GM-CSF, mannose-binding lectin, and factor H.

conclusionsThese results suggest that the presence of pentraxins and their ligands regulate macrophage differentiation in the blood and tissues, and that CRP may be a potent inducer of the anti-inflammatory cytokine IL-10.

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCell DifferentiationCells, CulturedComplement Factor HC-Reactive ProteinGranulocyte-Macrophage Colony-Stimulating FactorHumansInflammationInterleukin-10Macrophage ActivationMacrophagesMannose-Binding LectinsMonocytesN-Acetylneuraminic AcidAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenComplement Factor HC-Reactive ProteinGranulocyte-Macrophage Colony-Stimulating Factorhemoglobin-haptoglobin receptorInterleukin-10Mannose-Binding LectinsN-Acetylneuraminic AcidPentraxinsReceptors, Cell SurfaceSerum Amyloid P-ComponentSialic Acid Binding Ig-like Lectin 1C1qCRPFactor HInflammationMacrophageMannose binding lectinMBLMonocytePentraxinsPTX3SAP

Identifiers

PMID28619036
PMCPMC5472910
OpenAlexW2624733990

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.