Evidence map›Paper›PMID 12426151›Full record

ArticleEnvironmental health perspectives2002

Mercury-induced autoimmunity in mice.

Jesper Bo Nielsen, Per Hultman

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.1field-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

32 citing papers in PubMed, 94 citations in OpenAlex.

  1. Trial
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  6. Thymodepressin-Unforeseen Immunosuppressor.Molecules (Basel, Switzerland) · 2021
    Article
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  12. Biomarkers of mercury toxicity: Past, present, and future trends.Journal of toxicology and environmental health. Part B, Critical reviews · 2017
    Review
  13. Article
  14. Article
  15. Review
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  17. Low-dose mercury heightens early innate response to coxsackievirus infection in female mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
    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

2 authors at 1 institution in 1 country.

Jesper Bo NielsenEnvironmental Medicine, University of Southern Denmark, Winslowparken 17, DK-5000 Odense C, Denmark. jbnielsen@health.sdu.dk
Per Hultman
University of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have studied the effect of gender, genetics, and toxicokinetics on immune parameters in mercury-induced autoimmunity in mice. Data strongly suggest that the mechanism for mercury-induced autoimmunity involves modification of the autoantigen fibrillarin by mercury followed by a T-cell-dependent immune response driven by the modified fibrillarin. Mice with different H-2 haplotypes were treated with (203)HgCl(2) in a dose of 0.5-16 mg Hg/L drinking water for 10 weeks. Whole-body accumulation and renal accumulation of mercury were assessed. Serum antinuclear antibodies were used to evaluate the autoimmune response, and serum immunoglobulin E (IgE) to study effects on T-helper cells of type 2. Strains with a susceptible H-2 haplotype developed autoantibodies to the nucleolar protein fibrillarin (AFA) in a dose-dependent pattern within 2 weeks. The substantially lower whole-body and organ mercury level needed to induce AFA in the susceptible A.SW strain compared with the H-2 congenic B10.S strain demonstrates that genetic factors outside the H-2 region modify the autoimmune response. Mouse strains without the susceptible haplotype did not develop any autoimmune reaction irrespective of dose and organ deposition of mercury. In susceptible mouse strains, males and females had different thresholds for induction of autoimmune reactions. In susceptible strains, serum IgE increased dose dependently and reached a maximum after 1-2.5 weeks. A susceptible H-2 haplotype is therefore a prerequisite for the autoimmune response. Mercury exposure will modulate the response, qualitatively through the existence of dose-related thresholds for autoimmune response and quantitatively as increasing doses cause increasing autoimmune response. Further, gender and non-H-2 genes modulate both the induction and subsequent development of AFA. Induction of IgE seems not to be mechanistically linked to the AFA response.

Indexed as

AnimalsAutoimmune DiseasesChromosomal Proteins, Non-HistoneDisease Models, AnimalEnvironmental PollutantsFemaleGenetic Predisposition to DiseaseHaplotypesImmunoglobulin EKineticsMaleMercuryMiceMice, Inbred StrainsSex FactorsChromosomal Proteins, Non-HistoneEnvironmental PollutantsfibrillarinImmunoglobulin EMercury

Identifiers

PMID12426151
PMCPMC1241265
OpenAlexW2029498999

What OpenQuestion holds

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Registered trials

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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.