Evidence map›Paper›PMID 28960214›Full record

ArticleExperimental & molecular medicine2017

Upregulation of FcγRIIB by resveratrol via NF-κB activation reduces B-cell numbers and ameliorates lupus.

Jyun-Pei Jhou, Se-Jie Chen, Ho-Yin Huang, Wan-Wan Lin, Duen-Yi Huang, Shiang-Jong Tzeng

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2017. 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
1.7field-weighted citation impact, top 15% 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, 38 citations in OpenAlex.

  1. Article
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  10. Acta pharmaceutica Sinica. B · 2024
    Review
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  12. Article
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  15. Sirtuin family in autoimmune diseases.Frontiers in immunology · 2023
    Review
  16. Review
  17. Article
  18. Long-Term Hypermethylation ofJournal of clinical medicine · 2021
    Article
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  20. Review
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

6 authors at 1 institution in 1 country.

Jyun-Pei JhouDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Se-Jie ChenDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ho-Yin HuangDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wan-Wan LinDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Duen-Yi HuangDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shiang-Jong TzengDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resveratrol, an anti-inflammatory agent, can inhibit pro-inflammatory mediators by activating Sirt1, which is a class III histone deacetylase. However, whether resveratrol can regulate inhibitory or anti-inflammatory molecules has been less studied. FcγRIIB, a receptor for IgG, is an essential inhibitory receptor of B cells for blocking B-cell receptor-mediated activation and for directly inducing apoptosis of B cells. Because mice deficient in either Sirt1 or FcγRIIB develop lupus-like diseases, we investigated whether resveratrol can alleviate lupus through FcγRIIB. We found that resveratrol enhanced the expression of FcγRIIB in B cells, resulting in a marked depletion of plasma cells in the spleen and notably in the bone marrow, thereby decreasing serum autoantibody titers in MRL/lpr mice. The upregulation of FcγRIIB by resveratrol involved an increase of Sirt1 protein and deacetylation of p65 NF-κB (K310). Moreover, increased binding of phosphor-p65 NF-κB (S536) but decreased association of acetylated p65 NF-κB (K310) and phosphor-p65 NF-κB (S468) to the -480 promoter region of Fcgr2b gene was responsible for the resveratrol-mediated enhancement of FcγRIIB gene transcription. Consequently, B cells, especially plasma cells, were considerably reduced in MRL/lpr mice, leading to improvement of nephritis and prolonged survival. Taken together, we provide evidence that pharmacological upregulation of FcγRIIB expression in B cells via resveratrol can selectively reduce B cells, decrease serum autoantibodies and ameliorate lupus nephritis. Our findings lead us to propose FcγRIIB as a new target for therapeutic exploitation, particularly for lupus patients whose FcγRIIB expression levels in B cells are downregulated.

Indexed as

AnimalsAnti-Inflammatory AgentsAutoantibodiesB-LymphocytesCell MembraneDisease Models, AnimalGene Expression RegulationLupus Erythematosus, SystemicLupus NephritisMiceMice, Inbred MRL lprModels, BiologicalMyeloid CellsNF-kappa BPromoter Regions, GeneticReceptors, IgGAnti-Inflammatory AgentsAutoantibodiesFcgr2b protein, mouseNF-kappa BReceptors, IgGResveratrolStilbenes

Identifiers

PMID28960214
PMCPMC5628277
OpenAlexW2761292828

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.