Evidence map›Paper›PMID 20407433›Full record

ArticleThe American journal of gastroenterology2010

Autoantibodies against the exocrine pancreas in autoimmune pancreatitis: gene and protein expression profiling and immunoassays identify pancreatic enzymes as a major target of the inflammatory process.

J-Matthias Löhr, Ralf Faissner, Dirk Koczan, Peter Bewerunge, Claudio Bassi, Benedikt Brors, Roland Eils, Luca Frulloni, Anette Funk, Walter Halangk and 18 more

Erratum issuedAbstract read
In one paragraph

Article in The American journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 152 citations in OpenAlex.

  1. Article
  2. Review
  3. Risk of Pancreatic Cancer in Inflammatory Pancreatic Diseases.The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2025
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  6. Article
  7. Observational
  8. Review
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  11. Article
  12. Review
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  14. Article
  15. Article
  16. IgG4-related diseases of the digestive tract.Nature reviews. Gastroenterology & hepatology · 2022
    Review
  17. Review
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
    Jesnowski, Ralf [corrected to Jesenofsky, Ralf]
5 · Who and what money

Authors and funding

28 authors at 8 institutions in 4 countries.

J-Matthias LöhrMolecular Gastroenterology, German Cancer Research Center, Heidelberg, Germany. matthias.lohr@ki.se
Ralf Faissner
Dirk Koczan
Peter Bewerunge
Claudio Bassi
Benedikt Brors
Roland Eils
Luca Frulloni
Anette Funk
Walter Halangk
Ralf Jesenofsky
Ralf Jesnowski
Lars Kaderali
Jörg Kleeff
Burkhard Krüger
Markus M Lerch
Ralf Lösel
Mauro Magnani
Michael Neumaier
Stephanie Nittka
Miklós Sahin-Tóth
Julian Sänger
Sonja Serafini
Martina Schnölzer
Hermann-Josef Thierse
Silke Wandschneider
Giuseppe Zamboni
Günter Klöppel
Heidelberg University · DEGerman Cancer Research Center · DEUniversity of Verona · ITUniversity of Rostock · DEBoston University · USKiel University · DEUniversity Hospital Magdeburg · DEUniversity of Urbino · IT

Funding

Molecular Pathomechanism of Hereditary PancreatitisR01DK058088 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2001 to 2019
$5.3M
NIDDK NIH HHS R01 DK058088
6 · The paper itself

Abstract

objectivesAutoimmune pancreatitis (AIP) is thought to be an immune-mediated inflammatory process, directed against the epithelial components of the pancreas. The objective was to identify novel markers of disease and to unravel the pathogenesis of AIP.

methodsTo explore key targets of the inflammatory process, we analyzed the expression of proteins at the RNA and protein level using genomics and proteomics, immunohistochemistry, western blot, and immunoassay. An animal model of AIP with LP-BM5 murine leukemia virus-infected mice was studied in parallel. RNA microarrays of pancreatic tissue from 12 patients with AIP were compared with those of 8 patients with non-AIP chronic pancreatitis.

resultsExpression profiling showed 272 upregulated genes, including those encoding for immunoglobulins, chemokines and their receptors, and 86 downregulated genes, including those for pancreatic proteases such as three trypsinogen isoforms. Protein profiling showed that the expression of trypsinogens and other pancreatic enzymes was greatly reduced. Immunohistochemistry showed a near-loss of trypsin-positive acinar cells, which was also confirmed by western blotting. The serum of AIP patients contained high titers of autoantibodies against the trypsinogens PRSS1 and PRSS2 but not against PRSS3. In addition, there were autoantibodies against the trypsin inhibitor PSTI (the product of the SPINK1 gene). In the pancreas of AIP animals, we found similar protein patterns and a reduction in trypsinogen.

conclusionsThese data indicate that the immune-mediated process characterizing AIP involves pancreatic acinar cells and their secretory enzymes such as trypsin isoforms. Demonstration of trypsinogen autoantibodies may be helpful for the diagnosis of AIP.

Indexed as

AdultAnimalsAutoantibodiesAutoimmune DiseasesBlotting, WesternEnzyme-Linked Immunosorbent AssayFemaleGene Expression ProfilingHumansImmunoassayImmunohistochemistryInflammationLogistic ModelsMaleMiceMiddle AgedAutoantibodiesProteomeTrypsinogen

Identifiers

PMID20407433
PMCPMC3099227
OpenAlexW2019256148

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.