Evidence map›Paper›PMID 19289270›Full record

ArticleJournal of autoimmunity2009

Homing of GAD65 specific autoimmunity and development of insulitis requires expression of both DQ8 and human GAD65 in transgenic mice.

Raya B Elagin, Sadguna Balijepalli, Maria J Diacovo, Steinunn Baekkeskov, Juan C Jaume

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Pearls in autoimmunity.Auto- immunity highlights · 2011
    Review
  7. A contemporary update on scleroderma.Clinical reviews in allergy & immunology · 2011
    Article
  8. Food safety.Clinical reviews in allergy & immunology · 2010
    Review
  9. Article
  10. Mold and human health: separating the wheat from the chaff.Clinical reviews in allergy & immunology · 2010
    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

5 authors at 2 institutions in 1 country.

Raya B ElaginEndocrinology, Diabetes and Metabolism Section, Department of Medicine, School of Medicine, University of Wisconsin-Madison, Madison, WI 53792-5148, USA.
Sadguna Balijepalli
Maria J Diacovo
Steinunn Baekkeskov
Juan C Jaume
University of Wisconsin–Madison · USUniversity of California, San Francisco · US

Funding

Antigen Specific Immunity in Type 1 DiabetesR03DK064188 · NIDDK · UNIVERSITY OF WISCONSIN MADISON · PI JAUME, JUAN · 2003 to 2005
$443k
An Animal Model for Graves'Disease/OphthalmopathyR03EY014962 · NEI · UNIVERSITY OF WISCONSIN MADISON · PI JAUME, JUAN · 2003 to 2005
$378k
NEI NIH HHS R03 EY014962NIDDK NIH HHS R03 DK064188
6 · The paper itself

Abstract

MHC-class II genes determine susceptibility in human type-1 diabetes. In their context, presentation of target antigen(s) results in autoimmunity and beta-cell destruction. An animal model, in which human beta-cell autoantigen(s) are presented to effector cells in the context of human MHC-class II diabetes-susceptibility genes, would be desirable for studying molecular mechanisms of disease and developing antigen-specific immune-interventions. We report the development of antigen-specific insulitis in double-transgenic mice carrying the HLA-DQ8 diabetes-susceptibility haplotype and expressing the human autoantigen GAD65 in pancreatic beta-cells. Immunization with human GAD65 cDNA resulted in severe insulitis and low antibody levels in double-transgenic mice while control mice were mostly insulitis free. CFA/protein immunization resulted in high antibody levels and modest insulitis. Pancreatic lymphocytic infiltration progressed through stages (exocrine pancreas followed by peri- and intra-insulitis). Adoptive transfer of splenocytes from DNA-immunized mice resulted in development of insulitis in recipient transgenics. Our results show that immunization with a clinically relevant, type-1 diabetes human autoantigen, in a humanized genetic setting, results in the development of an immune response that homes to islets of Langerhans. This animal model will facilitate studies of autoimmunity to GAD65 in the context of HLA-DQ8, and development of methods to induce tolerance and prevent insulitis.

Indexed as

Adoptive TransferAnimalsAutoantibodiesAutoantigensCell ProliferationCloning, MolecularDiabetes Mellitus, Type 1Disease Models, AnimalDisease ProgressionGenetic Predisposition to DiseaseGlutamate DecarboxylaseHLA-DQ AntigensHumansImmune ToleranceMiceMice, Inbred C57BLAutoantibodiesAutoantigensGlutamate Decarboxylaseglutamate decarboxylase 2HLA-DQ8 antigenHLA-DQ Antigens

Identifiers

PMID19289270
PMCPMC2705176
OpenAlexW2069031096

What OpenQuestion holds

Textmetadata
LicenceTDM
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.