Evidence map›Paper›PMID 29410669›Full record

ArticleFrontiers in immunology2018

Lactoferrin-Containing Immunocomplexes Drive the Conversion of Human Macrophages from M2- into M1-like Phenotype.

Chen-Hui Gao, Hong-Liang Dong, Li Tai, Xiao-Ming Gao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

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  14. Identifying novel mechanisms of abdominal aortic aneurysmFrontiers in cardiovascular medicine · 2022
    Article
  15. Kidney protective potential of lactoferrin: pharmacological insights and therapeutic advances.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
    Review
  16. Article
  17. Immune Actions on the Peripheral Nervous System in Pain.International journal of molecular sciences · 2021
    Review
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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

4 authors at 1 institution in 1 country.

Chen-Hui GaoInstitute of Biology and Medical Sciences, Soochow University, Suzhou, China.
Hong-Liang DongInstitute of Biology and Medical Sciences, Soochow University, Suzhou, China.
Li TaiInstitute of Biology and Medical Sciences, Soochow University, Suzhou, China.
Xiao-Ming GaoInstitute of Biology and Medical Sciences, Soochow University, Suzhou, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are multifunctional cells that perform diverse roles in health and disease and considered the main source of inflammatory cytokines in affected joints of patients with rheumatoid arthritis (RA). M2 macrophages are well known as anti-inflammation and wound-healing cells; however, recent evidence suggests that they can also promote inflammation in RA, although the underlying mechanism remains to be clarified. Based upon our recent finding that lactoferrin (LTF)-containing IgG immunocomplex (LTF-IC), found elevated in RA sera, potent activators of human monocytes/macrophages, we herein demonstrate that LTF-IC was able to elicit immediate proinflammatory cytokine production by M2-polarized human macrophages through coligation with CD14/toll-like receptor (TLR) 4 and FcγRIIa (CD32a). The LTF-IC-treated M2 cells adopted surface maker expression profile similar to that of M1 phenotype and became functionally hyperactive to subsequent stimuli such as lipopolysaccharide, zymosan and IL-1β, which could provide a positive feedback signal to promote excessive inflammation in RA. They also acquired the ability to facilitate activation of Th17 cells that are known to play critical roles in RA pathology. We propose that IgG ICs containing TLR agonizing autoantigens are able to directly switch human macrophages from M2 into M1-like phenotype, thereby promoting excessive inflammation in autoimmune diseases such as RA.

Indexed as

Arthritis, RheumatoidCells, CulturedHumansImmunoglobulin GInterleukin-1betaLactoferrinLipopolysaccharidesLymphocyte ActivationMacrophagesReceptors, IgGTh17 CellsToll-Like Receptor 4ZymosanFc gamma receptor IIAIL1B protein, humanImmunoglobulin GInterleukin-1betaLactoferrinLipopolysaccharidesReceptors, IgGTLR4 protein, humanToll-Like Receptor 4Zymosanhyperactivityimmune complexlactoferrinM2 macrophagesrheumatoid arthritis

Identifiers

PMID29410669
PMCPMC5787126
OpenAlexW2788931403

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.