Evidence map›Paper›PMID 7533789›Full record

ArticleThe Journal of clinical investigation1995

Epstein-Barr virus-induced autoimmune responses. II. Immunoglobulin G autoantibodies to mimicking and nonmimicking epitopes. Presence in autoimmune disease.

J H Vaughan, M D Nguyen, J R Valbracht, K Patrick, G H Rhodes

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
4.3field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Endogenous retroviral pathogenesis in lupus.Current opinion in rheumatology · 2010
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mechanisms of viral pathogenesis in rheumatic disease.Annals of the rheumatic diseases · 1999
    Review
  17. Article
  18. Article
  19. Epitope spreading.Current opinion in immunology · 1996
    Review
  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 2 institutions in 1 country.

J H VaughanDepartment of Medicine, University of California, San Diego, La Jolla 92093-0663.
M D Nguyen
J R Valbracht
K Patrick
G H Rhodes
University of California San Diego · USSan Diego State University · US

Funding

THE EPSTEIN-BARR VIRUS AND AUTOIMMUNE DISEASER01AR021175 · NIAMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI VAUGHAN, JOHN H · 1986 to 1992
–
NIAMS NIH HHS AR21175
6 · The paper itself

Abstract

During infectious mononucleosis, IgM autoantibodies are generated to a protein, p542, which contains a glycine-rich 28-mer epitope cross-reactive with the Epstein-Barr nuclear antigen-1 through Epstein-Barr nuclear antigen-1's glycine/alanine repeat. In normal individuals it is uncommon to find IgG anti-p542, but among patients with progressive systemic sclerosis, systemic lupus erythematosus, and ulcerative colitis high IgG anti-p542 (> 3 SD above the mean of normal 20-50 yr controls) occurred frequently. Lesser elevations occurred in Sjögren's syndrome, rheumatoid arthritis, ankylosing spondylitis, and Crohn's disease, but none with chronic hepatitis B infection. The reactive epitopes on p542 were mapped with deletion mutants, which indicated that the glycine-rich 28-mer was the major antigenic determinant, with lesser antibody responses to other epitopes. We conclude that normally there is an inability to generate IgG autoantibodies to the cross-reactive (mimicking) epitope of the p542 host protein, but that this inability is overcome in a proportion of patients with autoimmune disease. We conclude also that non-cross-reactive autoepitopes exist on p542 protein, to which IgG autoantibodies can commonly be formed in autoimmune disorders. The mechanisms responsible for the latter must involve different mechanisms than those responsible for autoantibodies to the mimicking epitope.

Indexed as

AdolescentAdultAgedAmino Acid SequenceAntigens, ViralAutoantigensAutoimmune DiseasesAutoimmunityConvalescenceCross ReactionsDNA-Binding ProteinsEpitopesEpstein-Barr Virus Nuclear AntigensHumansImmunoglobulin GInfectious MononucleosisAntigens, ViralAutoantigensDNA-Binding ProteinsEpitopesEpstein-Barr Virus Nuclear AntigensImmunoglobulin Gp542 autoantigen

Identifiers

PMID7533789
PMCPMC441471
OpenAlexW2011827738

What OpenQuestion holds

Textmetadata
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.