Evidence map›Paper›PMID 28333576›Full record

ArticleViral immunology2017

Epstein-Barr Virus Lytic Reactivation Activates B Cells Polyclonally and Induces Activation-Induced Cytidine Deaminase Expression: A Mechanism Underlying Autoimmunity and Its Contribution to Graves' Disease.

Keiko Nagata, Keisuke Kumata, Yuji Nakayama, Yukio Satoh, Hirotsugu Sugihara, Sayuri Hara, Michiko Matsushita, Satoshi Kuwamoto, Masako Kato, Ichiro Murakami and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Viral immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Review
  6. Article
  7. Review
  8. Article
  9. The Role of Exposomes in the Pathophysiology of Autoimmune Diseases II: Pathogens.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022
    Review
  10. Article
  11. IgG4 as a Biomarker in Graves' Orbitopathy.Mediators of inflammation · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Stress, pseudoallergens, autoimmunity, infection and inflammation in chronic spontaneous urticaria.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    Review
  17. Article
  18. Article
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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

11 authors at 2 institutions in 1 country.

Keiko Nagata1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Keisuke Kumata1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Yuji Nakayama2 Division of Functional Genomics, Research Center for Bioscience and Technology, Tottori University , Yonago, Japan .
Yukio Satoh3 Division of Biosignaling, Department of Biomedical Sciences, Faculty of Medicine, Tottori University , Yonago, Japan .
Hirotsugu Sugihara1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Sayuri Hara1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Michiko Matsushita1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Satoshi Kuwamoto1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Masako Kato1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Ichiro Murakami4 Department of Pathology, Kochi University Medical School Medical Course , Nankoku-shi, Japan .
Kazuhiko Hayashi1 Division of Molecular Pathology, Department of Pathology, Faculty of Medicine, Tottori University , Yonago, Japan .
Tottori University · JPKochi Medical School Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Graves' disease is an autoimmune disease that results in and is the most common cause of hyperthyroidism, and the reactivation of persisting Epstein-Barr virus (EBV) in B lymphocytes induces the differentiation of host B cells into plasma cells. We previously reported that some EBV-infected B cells had thyrotropin receptor antibodies (TRAbs) as surface immunoglobulins (Igs), and EBV reactivation induced these TRAb+EBV+ cells to produce TRAbs. EBV reactivation induces Ig production from host B cells. The purpose of the present study was to examine total Ig productions from B cell culture fluids and to detect activation-induced cytidine deaminase (AID), nuclear factor kappa B (NF-κB), and EBV latent membrane protein (LMP) 1 in culture B cells during EBV reactivation induction and then we discussed the mechanisms of EBV reactivation-induced Ig production in relation to autoimmunity. We showed that the EBV reactivation induces the production of every isotype of Ig and suggested that the Ig production was catalyzed by AID through LMP1 and NF-κB. The results that the amount of IgM was significantly larger compared with IgG suggested the polyclonal B cell activation due to LMP1. We proposed the pathway of EBV reactivation induced Ig production; B cells newly infected with EBV are activated by polyclonal B cell activation and produce Igs through plasma cell differentiation induced by EBV reactivation. LMP1-induced AID enabled B cells to undergo class-switch recombination to produce every isotype of Ig. According to this mechanism, EBV rescues autoreactive B cells to produce autoantibodies, which contribute to the development and exacerbation of autoimmune diseases.

Indexed as

AutoimmunityLymphocyte ActivationVirus ActivationAdultB-LymphocytesCells, CulturedCytidine DeaminaseFemaleGraves DiseaseHerpesvirus 4, HumanHumansImmunoglobulin GImmunoglobulin MMaleMiddle AgedNF-kappa BCytidine DeaminaseEBV-associated membrane antigen, Epstein-Barr virusImmunoglobulin GImmunoglobulin MNF-kappa BViral Matrix Proteinsactivation-induced cytidine deaminaseautoreactive B cellsEpstein–Barr virusGraves' diseasepolyclonal B cell activationreactivation

Identifiers

PMID28333576
PMCPMC5393416
OpenAlexW2607495927

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.