Evidence map›Paper›PMID 22174447›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Helminth protection against autoimmune diabetes in nonobese diabetic mice is independent of a type 2 immune shift and requires TGF-β.

Marc P Hübner, Yinghui Shi, Marina N Torrero, Ellen Mueller, David Larson, Kateryna Soloviova, Fabian Gondorf, Achim Hoerauf, Kristin E Killoran, J Thomas Stocker and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Transient Depletion of Foxp3Frontiers in immunology · 2021
    Article
  9. Review
  10. Article
  11. AxenicJournal of translational autoimmunity · 2020
    Article
  12. The Gastrointestinal HelminthFrontiers in immunology · 2020
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

13 authors at 3 institutions in 2 countries.

Marc P HübnerDepartment of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Yinghui Shi
Marina N Torrero
Ellen Mueller
David Larson
Kateryna Soloviova
Fabian Gondorf
Achim Hoerauf
Kristin E Killoran
J Thomas Stocker
Stephen J Davies
Kristin V Tarbell
Edward Mitre
Uniformed Services University of the Health Sciences · USUniversity Hospital Bonn · DENational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Protection against Type I diabetes by parasitic helminthsDP2DK083131 · NIDDK · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI MITRE, EDWARD E · 2008 to 2008
$2.3M
NIDDK NIH HHS 1DP2DK083131NIDDK NIH HHS DP2 DK083131
6 · The paper itself

Abstract

Leading hypotheses to explain helminth-mediated protection against autoimmunity postulate that type 2 or regulatory immune responses induced by helminth infections in the host limit pathogenic Th1-driven autoimmune responses. We tested these hypotheses by investigating whether infection with the filarial nematode Litomosoides sigmodontis prevents diabetes onset in IL-4-deficient NOD mice and whether depletion or absence of regulatory T cells, IL-10, or TGF-β alters helminth-mediated protection. In contrast to IL-4-competent NOD mice, IL-4-deficient NOD mice failed to develop a type 2 shift in either cytokine or Ab production during L. sigmodontis infection. Despite the absence of a type 2 immune shift, infection of IL-4-deficient NOD mice with L. sigmodontis prevented diabetes onset in all mice studied. Infections in immunocompetent and IL-4-deficient NOD mice were accompanied by increases in CD4(+)CD25(+)Foxp3(+) regulatory T cell frequencies and numbers, respectively, and helminth infection increased the proliferation of CD4(+)Foxp3(+) cells. However, depletion of CD25(+) cells in NOD mice or Foxp3(+) T cells from splenocytes transferred into NOD.scid mice did not decrease helminth-mediated protection against diabetes onset. Continuous depletion of the anti-inflammatory cytokine TGF-β, but not blockade of IL-10 signaling, prevented the beneficial effect of helminth infection on diabetes. Changes in Th17 responses did not seem to play an important role in helminth-mediated protection against autoimmunity, because helminth infection was not associated with a decreased Th17 immune response. This study demonstrates that L. sigmodontis-mediated protection against diabetes in NOD mice is not dependent on the induction of a type 2 immune shift but does require TGF-β.

Indexed as

AnimalsDiabetes Mellitus, Type 1FemaleFilariasisFilarioideaInterleukin-10Interleukin-4MiceMice, 129 StrainMice, Inbred NODMice, KnockoutMice, TransgenicTh1 CellsT-Lymphocytes, RegulatoryTransforming Growth Factor betaIL10 protein, mouseInterleukin-10Interleukin-4Transforming Growth Factor beta

Identifiers

PMID22174447
PMCPMC3253252
OpenAlexW2151178653

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.