Evidence map›Paper›PMID 25603827›Full record

ArticleMucosal immunology2015

Gastric LTi cells promote lymphoid follicle formation but are limited by IRAK-M and do not alter microbial growth.

J Shiu, M B Piazuelo, H Ding, S J Czinn, M L Drakes, A Banerjee, N Basappa, K S Kobayashi, W F Fricke, T G Blanchard

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. ILCs-Crucial Players in Enteric Infectious Diseases.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

10 authors at 4 institutions in 1 country.

J ShiuDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
M B PiazueloDepartment of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
H DingDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
S J CzinnDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
M L DrakesCardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, Illinois, USA.
A BanerjeeDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
N BasappaDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
K S KobayashiDepartment of Microbial and Molecular Pathogenesis, Texas A & M Health Science Center, Texas, USA.
W F FrickeInstitute for Genomic Sciences, University of Maryland, Baltimore, Maryland, USA.
T G BlanchardDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
University of Maryland, Baltimore · USLoyola University Chicago · USTexas A&M Health Science Center · USVanderbilt University · US

Funding

Project 3 - Molecular Signatures of Gastric Carcinogenesis in the Host Response to H. pyloriP01CA028842 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, KEITH T. · 1985 to 2019
$15.8M
Mucosal Immunology of Heliobacter Induced GastritisR01DK046461 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI CZINN, STEVEN J · 1994 to 2011
$3.6M
H. PYLORI-SPECIFIC REGULATORY T CELLS THAT LIMIT HOST RESPONSER01AI055710 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BLANCHARD, THOMAS G · 2004 to 2008
$1.1M
Canadian Institutes of Health Research DFSA-236840NCI NIH HHS P01 CA028842NIAID NIH HHS R01 AI055710NIAID NIH HHS R01-AI-055710NIDDK NIH HHS R01 DK046461NIDDK NIH HHS R01-DK-46461
6 · The paper itself

Abstract

Lymphoid tissue inducer (LTi) cells are activated by accessory cell IL-23, and promote lymphoid tissue genesis and antibacterial peptide production by the mucosal epithelium. We investigated the role of LTi cells in the gastric mucosa in the context of microbial infection. Mice deficient in IRAK-M, a negative regulator of TLR signaling, were investigated for increased LTi cell activity, and antibody mediated LTi cell depletion was used to analyze LTi cell dependent antimicrobial activity. H. pylori infected IRAK-M deficient mice developed increased gastric IL-17 and lymphoid follicles compared to wild type mice. LTi cells were present in naive and infected mice, with increased numbers in IRAK-M deficient mice by two weeks. Helicobacter and Candida infection of LTi cell depleted rag1(-/-) mice demonstrated LTi-dependent increases in calprotectin but not RegIII proteins. However, pathogen and commensal microbiota populations remained unchanged in the presence or absence of LTi cell function. These data demonstrate LTi cells are present in the stomach and promote lymphoid follicle formation in response to infection, but are limited by IRAK-M expression. Additionally, LTi cell mediated antimicrobial peptide production at the gastric epithelium is less efficacious at protecting against microbial pathogens than has been reported for other tissues.

Indexed as

AnimalsCandidaCandidiasisGastric MucosaHelicobacterHelicobacter InfectionsHomeodomain ProteinsInterleukin-1 Receptor-Associated KinasesInterleukin-23Lymphoid TissueMiceMice, KnockoutHomeodomain ProteinsInterleukin-1 Receptor-Associated KinasesInterleukin-23Irak3 protein, mouseRAG-1 protein

Identifiers

PMID25603827
PMCPMC4510039
OpenAlexW2075467122

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.