Evidence map›Paper›PMID 8577709›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

A role of Hsp60 in autoimmune diabetes: analysis in a transgenic model.

O S Birk, D C Douek, D Elias, K Takacs, H Dewchand, S L Gur, M D Walker, R van der Zee, I R Cohen, D M Altmann

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of Heat Shock Proteins in Glaucoma.International journal of molecular sciences · 2019
    Review
  4. Suppressed heat shock protein response in the kidney of exercise-trained diabetic rats.Scandinavian journal of medicine & science in sports · 2018
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Evidence for a primary islet autoantigen (preproinsulin 1) for insulitis and diabetes in the nonobese diabetic mouse.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  17. Transgenic models of autoimmune disease.Clinical and experimental immunology · 2002
    Review
  18. Review
  19. 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

10 authors at 3 institutions in 2 countries.

O S BirkMedical Research Council Clinical Sciences Centre, Royal Postgraduate Medical School, Hammersmith Hospital, London, United Kingdom.
D C Douek
D Elias
K Takacs
H Dewchand
S L Gur
M D Walker
R van der Zee
I R Cohen
D M Altmann
Medical Research Council · GBHammersmith Hospital · GBWeizmann Institute of Science · IL

Funding

Wellcome Trust
6 · The paper itself

Abstract

A pathogenic role for self-reactive cells against the stress protein Hsp60 has been proposed as one of the events leading to autoimmune destruction of pancreatic beta cells in the diabetes of nonobese diabetic (NOD) mice. To examine this hypothesis, we generated transgenic NOD mice carrying a murine Hsp60 transgene driven by the H-2E alpha class II promoter. This would be expected to direct expression of the transgene to antigen-presenting cells including those in the thymus and so induce immunological tolerance by deletion. Detailed analysis of Hsp60 expression revealed that the endogenous gene is itself expressed strongly in thymic medullary epithelium (and weakly in cortex) yet fails to induce tolerance. Transgenic mice with retargeted Hsp60 showed overexpression of the gene in thymic cortical epithelium and in bone marrow-derived cells. Analysis of spontaneous T-cell responses to a panel of self and heterologous Hsp60 antigens showed that tolerance to the protein had not been induced, although responses to an immunodominant 437-460 epitope implicated in disease were suppressed, probably indicating an epitope shift. This correlated with changes in disease susceptibility: insulitis in transgenic mice was substantially reduced so that pathology rarely progressed beyond periislet infiltration. This was reflected in a substantial reduction in hyperglycemia and disease. These data indicate that T cells specific for some epitopes of murine Hsp60 are likely to be involved in the islet-cell destruction that occurs in NOD mice.

Indexed as

Lymphocyte ActivationAnimalsChaperonin 60Diabetes Mellitus, Type 1Disease SusceptibilityFemaleGenes, MHC Class IIImmunity, CellularIslets of LangerhansMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, Inbred NODMice, TransgenicPolymerase Chain ReactionChaperonin 60Recombinant Proteins

Identifiers

PMID8577709
PMCPMC40025
OpenAlexW1976020265

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.