Evidence map›Paper›PMID 24345804›Full record

ArticleMucosal immunology2014

Hypertrophy of infected Peyer's patches arises from global, interferon-receptor, and CD69-independent shutdown of lymphocyte egress.

O Schulz, M Ugur, M Friedrichsen, K Radulovic, J-H Niess, S Jalkanen, A Krueger, O Pabst

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Lymphatic endothelial cells of the lymph node.Nature reviews. Immunology · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Lymph node γδ and αβ CD8Scientific reports · 2018
    Article
  11. Article
  12. CD69: from activation marker to metabolic gatekeeper.European journal of immunology · 2017
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. 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

8 authors at 4 institutions in 3 countries.

O SchulzInstitute of Immunology, Hannover Medical School, Hannover, Germany.
M UgurInstitute of Immunology, Hannover Medical School, Hannover, Germany.
M FriedrichsenInstitute of Immunology, Hannover Medical School, Hannover, Germany.
K RadulovicDepartment of Internal Medicine I, University of Ulm, Ulm, Germany.
J-H Niess1] Department of Internal Medicine I, University of Ulm, Ulm, Germany [2] Current address: Department of Visceral Surgery and Medicine, Inselspital, Bern, Switzerland.
S JalkanenMediCity Research Laboratory, Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
A KruegerInstitute of Immunology, Hannover Medical School, Hannover, Germany.
O PabstInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DEUniversität Ulm · DEUniversity Hospital of Bern · CHUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymphoid organ hypertrophy is a hallmark of localized infection. During the inflammatory response, massive changes in lymphocyte recirculation and turnover boost lymphoid organ cellularity. Intriguingly, the exact nature of these changes remains undefined to date. Here, we report that hypertrophy of Salmonella-infected Peyer's patches (PPs) ensues from a global "shutdown" of lymphocyte egress, which traps recirculating lymphocytes in PPs. Surprisingly, infection-induced lymphocyte sequestration did not require previously proposed mediators of lymphoid organ shutdown including type I interferon receptor and CD69. In contrast, following T-cell receptor-mediated priming, CD69 was essential to selectively block CD4(+) effector T-cell egress. Our findings segregate two distinct lymphocyte sequestration mechanisms, which differentially rely on intrinsic modulation of lymphocyte egress capacity and inflammation-induced changes in the lymphoid organ environment.

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensHypertrophyLectins, C-TypeLigandsLymphocyte CountLymphocytesMiceMice, KnockoutMice, TransgenicPeyer's PatchesReceptors, InterferonSalmonellaSalmonella InfectionsAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensLectins, C-TypeLigandsReceptors, InterferonToll-Like Receptors

Identifiers

PMID24345804
PMCPMC4060605
OpenAlexW2048289368

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.