Evidence map›Paper›PMID 21801869›Full record

ArticleThe American journal of pathology2011

Manifestation of spontaneous and early autoimmune gastritis in CCR7-deficient mice.

Susann Winter, Armin Rehm, Katharina Wichner, Tobias Scheel, Arvind Batra, Britta Siegmund, Claudia Berek, Martin Lipp, Uta E Höpken

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Identification of a Novel OX40LScientific reports · 2018
    Article
  9. CXJournal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  10. CCR7 Deficiency Allows Accelerated Clearance ofJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  11. Induction of autoimmune disease by deletion of CTLA-4 in mice in adulthood.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  12. Article
  13. Review
  14. 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

9 authors at 3 institutions in 1 country.

Susann WinterDepartment of Tumor Genetics and Immunogenetics, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Armin Rehm
Katharina Wichner
Tobias Scheel
Arvind Batra
Britta Siegmund
Claudia Berek
Martin Lipp
Uta E Höpken
Max Delbrück Center · DECharité - Universitätsmedizin Berlin · DEGerman Rheumatism Research Centre · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune gastritis is a common autoimmune disorder characterized by chronic inflammatory cell infiltrates, atrophy of the corpus and fundus, and the occurrence of autoantibodies to parietal cell antigen. In CCR7-deficient mice, autoimmune gastritis developed spontaneously and was accompanied by metaplasia of the gastric mucosa and by the formation of tertiary lymphoid organs at gastric mucosal sites. T cells of CCR7-deficient mice showed an activated phenotype in the gastric mucosa, mesenteric lymph nodes, and peripheral blood. In addition, elevated serum IgG levels specific to gastric parietal cell antigen were detected. Because the role of organized lymphocytic aggregates at this inflammatory site is not completely understood, we first analyzed the cellular requirements for the formation of these structures. Autoreactive CD4(+) T cells were pivotal for tertiary lymphoid follicle formation, most likely in cooperation with dendritic cells, macrophages, and B cells. Second, we analyzed the necessity of secondary lymph nodes and tertiary lymphoid organs for the development of autoimmune gastritis using CCR7 single- and CCR7/lymphotoxin α double-deficient mice. Strikingly, manifestation of autoimmune gastritis was observed in the absence of secondary lymph nodes and preceded the development of tertiary lymphoid organs. Taken together, these findings identify an inflammatory process where gastric autoreactive T cells independent of organized tertiary lymphoid organs and classic lymph nodes can induce and maintain autoimmune gastritis.

Indexed as

AnimalsAutoimmune DiseasesBone Marrow CellsCD11c AntigenCD4-Positive T-LymphocytesDendritic CellsFlow CytometryGastric MucosaGastritisHydrogen-Ion ConcentrationImmunoglobulin GInterferon-gammaInterleukin-17Leukocytes, MononuclearMiceMice, Inbred C57BLCcr7 protein, mouseCD11c AntigenImmunoglobulin GInterferon-gammaInterleukin-17Receptors, CCR7

Identifiers

PMID21801869
PMCPMC3157176
OpenAlexW2144811427

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.