Evidence map›Paper›PMID 26325540›Full record

ArticlePloS one2015

Quantitative Trait Locus Analysis Implicates CD4⁺/CD44high Memory T Cells in the Pathogenesis of Murine Autoimmune Pancreatitis.

Julia Bischof, Sarah Müller, Luise Borufka, Farahnaz Asghari, Steffen Möller, Stephanie-Anna Holzhüter, Horst Nizze, Saleh M Ibrahim, Robert Jaster

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Frontiers in immunology · 2025
    Article
  2. Article
  3. Impact of diet and genes on murine autoimmune pancreatitis.Journal of cellular and molecular medicine · 2020
    Article
  4. Adoptive transfer of CD3Journal of cellular and molecular medicine · 2018
    Article
  5. 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.

Julia BischofDepartment of Dermatology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.
Sarah MüllerDepartment of Medicine II, Division of Gastroenterology, Rostock University Medical Center, E.-Heydemann-Str. 6, 18057 Rostock, Germany.
Luise BorufkaDepartment of Medicine II, Division of Gastroenterology, Rostock University Medical Center, E.-Heydemann-Str. 6, 18057 Rostock, Germany.
Farahnaz AsghariDepartment of Dermatology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany; Department of Medicine II, Division of Gastroenterology, Rostock University Medical Center, E.-Heydemann-Str. 6, 18057 Rostock, Germany.
Steffen MöllerDepartment of Dermatology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.
Stephanie-Anna HolzhüterInstitute of Pathology, Rostock University Medical Center, Strempelstr. 14, 18057 Rostock, Germany.
Horst NizzeInstitute of Pathology, Rostock University Medical Center, Strempelstr. 14, 18057 Rostock, Germany.
Saleh M IbrahimDepartment of Dermatology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.
Robert JasterDepartment of Medicine II, Division of Gastroenterology, Rostock University Medical Center, E.-Heydemann-Str. 6, 18057 Rostock, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mouse strain MRL/MpJ is prone to spontaneously develop autoimmune pancreatitis (AIP). To elucidate the genetic control towards the development of the phenotype and to characterize contributions of immunocompetent cell types, MRL/MpJ mice were interbred with three additional strains (BXD2/TYJ, NZM2410/J, CAST/EIJ) for four generations in an advanced intercross line. Cellular phenotypes were determined by flow cytometric quantification of splenic leukocytes and complemented by the histopathological evaluation of pancreatic lesions. An Illumina SNP array was used for genotyping. QTL analyses were performed with the R implementation of HAPPY. Out of 41 leukocyte subpopulations (B cells, T cells and dendritic cells), only three were significantly associated with AIP: While CD4+/CD44high memory T cells and CD4+/CD69+ T helper (Th) cells correlated positively with the disease, the cytotoxic T cell phenotype CD8+/CD44low showed a negative correlation. A QTL for AIP on chromosome 2 overlapped with QTLs for CD4+/CD44high and CD8+/CD44high memory T cells, FoxP3+/CD4+ and FoxP3+/CD8+ regulatory T cells (Tregs), and CD8+/CD69+ cytotoxic T cells. On chromosome 6, overlapping QTLs for AIP and CD4+/IL17+ Th17 cells and again FoxP3+/CD8+ Tregs were observed. In conclusion, CD4+/CD44high memory T cells are the only leukocyte subtype that could be linked to AIP both by correlation studies and from observed overlapping QTL. The potential role of this cell type in the pathogenesis of AIP warrants further investigations.

Indexed as

AnimalsAutoimmune DiseasesCD4-Positive T-LymphocytesFemaleFlow CytometryHyaluronan ReceptorsMaleMiceMice, Inbred StrainsPancreasPancreatitis, ChronicQuantitative Trait LociT-Lymphocyte SubsetsHyaluronan Receptors

Identifiers

PMID26325540
PMCPMC4556487

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.