Evidence map›Paper›PMID 18523243›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Spontaneous development of a pancreatic exocrine disease in CD28-deficient NOD mice.

Craig Meagher, Qizhi Tang, Brian T Fife, Helene Bour-Jordan, Jenny Wu, Cecile Pardoux, Mingying Bi, Kristin Melli, Jeffrey A Bluestone

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. 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
3.4field-weighted citation impact, top 9% 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, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Exploiting apoptosis for therapeutic tolerance induction.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Review
  10. Article
  11. Review
  12. Regulatory T-cell therapy in transplantation: moving to the clinic.Cold Spring Harbor perspectives in medicine · 2013
    Review
  13. The B7-independent isoform of CTLA-4 functions to regulate autoimmune diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Article
  14. Article
  15. Breakdown in peripheral tolerance in type 1 diabetes in mice and humans.Cold Spring Harbor perspectives in medicine · 2012
    Review
  16. Autoantibodies in autoimmune pancreatitis.International journal of rheumatology · 2012
    Article
  17. Article
  18. Article
  19. Article
  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

9 authors at 1 institution in 1 country.

Craig MeagherDiabetes Center, University of California, San Francisco, CA 94143, USA.
Qizhi Tang
Brian T Fife
Helene Bour-Jordan
Jenny Wu
Cecile Pardoux
Mingying Bi
Kristin Melli
Jeffrey A Bluestone
University of California, San Francisco · US

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2003 to 2019
$21.8M
UCSF Autoimmunity Center of ExcellenceU19AI056388 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WOFSY, DAVID · 2003 to 2013
$6.3M
Spontaneous Autoimmune Model of Peripheral NeuropathyR01AI050834 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BLUESTONE, JEFFREY A · 2002 to 2011
$3.1M
REGULATION OF BETA CELL DEATH IN THE PATHOGENESIS OF IDDMP01DK049799 · NIDDK · UNIVERSITY OF CHICAGO · PI SANT, ANDREA JANINE · 1995 to 1999
–
NIAID NIH HHS R01 AI050834NIAID NIH HHS R01 AI 50834-02NIAID NIH HHS U19 AI 056388NIAID NIH HHS U19 AI056388NIDDK NIH HHS P01 DK049799NIDDK NIH HHS P30 DK063720NIDDK NIH HHS P30 DK 63720
6 · The paper itself

Abstract

Autoimmune pancreatitis (AIP) is a heterogeneous autoimmune disease in humans characterized by a progressive lymphocytic and plasmacytic infiltrate in the exocrine pancreas. In this study, we report that regulatory T cell-deficient NOD.CD28KO mice spontaneously develop AIP that closely resembles the human disease. NOD mouse AIP was associated with severe periductal and parenchymal inflammation of the exocrine pancreas by CD4(+) T cells, CD8(+) T cells, and B cells. Spleen CD4(+) T cells were found to be both necessary and sufficient for the development of AIP. Autoantibodies and autoreactive T cells from affected mice recognized a approximately 50-kDa protein identified as pancreatic amylase. Importantly, administration of tolerogenic amylase-coupled fixed spleen cells significantly ameliorated disease severity, suggesting that this protein functions as a key autoantigen. The establishment and characterization of this spontaneous pancreatic amylase-specific AIP in regulatory T cell-deficient NOD.CD28KO mice provides an excellent model for the study of disease pathogenesis and development of new therapies for human autoimmune pancreatitis.

Indexed as

Adoptive Transferalpha-AmylasesAnimalsAutoantigensAutoimmune DiseasesCD28 AntigensCells, CulturedFemaleImmune ToleranceMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, KnockoutMice, Transgenicalpha-AmylasesAutoantigensCD28 Antigens

Identifiers

PMID18523243
PMCPMC2429990
OpenAlexW1951212234

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.