Evidence map›Paper›PMID 19188681›Full record

ArticleThe Journal of clinical investigation2009

Highly purified Th17 cells from BDC2.5NOD mice convert into Th1-like cells in NOD/SCID recipient mice.

David Bending, Hugo De la Peña, Marc Veldhoen, Jenny M Phillips, Catherine Uyttenhove, Brigitta Stockinger, Anne Cooke

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 286 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
286citing papers in PubMed, 2 pooled it
45.7field-weighted citation impact, top 1% 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

286 citing papers in PubMed, 2 syntheses or guidelines pooled it, 541 citations in OpenAlex.

  1. Pooled it
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  6. Aiolos and Eos drive distinct human TH17 functional states.Cellular and molecular life sciences : CMLS · 2026
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226 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

David BendingDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom.
Hugo De la Peña
Marc Veldhoen
Jenny M Phillips
Catherine Uyttenhove
Brigitta Stockinger
Anne Cooke
University of Cambridge · GBLudwig Cancer Research · BE

Funding

Biotechnology and Biological Sciences Research CouncilWellcome Trust
6 · The paper itself

Abstract

Th17 cells are involved in the pathogenesis of many autoimmune diseases, but it is not clear whether they play a pathogenic role in type 1 diabetes. Here we investigated whether mouse Th17 cells with specificity for an islet antigen can induce diabetes upon transfer into NOD/SCID recipient mice. Induction of diabetes in NOD/SCID mice via adoptive transfer of Th1 cells from BDC2.5 transgenic mice was prevented by treatment of the recipient mice with a neutralizing IFN-γ-specific antibody. This result suggested a major role of Th1 cells in the induction of disease in this model of type 1 diabetes. Nevertheless, transfer of highly purified Th17 cells from BDC2.5 transgenic mice caused diabetes in NOD/SCID recipients with similar rates of onset as in transfer of Th1 cells. However, treatment with neutralizing IL-17-specific antibodies did not prevent disease. Instead, the transferred Th17 cells, completely devoid of IFN-γ at the time of transfer, rapidly converted to secrete IFN-γ in the NOD/SCID recipients. Purified Th17 cells also upregulated Tbet and secreted IFN-γ upon exposure to IL-12 in vitro and in vivo in NOD/SCID recipients. These results indicate substantial plasticity of Th17 commitment toward a Th1-like profile.

Indexed as

Adoptive TransferAnimalsAntibodies, MonoclonalBasic Helix-Loop-Helix ProteinsBlood GlucoseCell DifferentiationDiabetes Mellitus, Type 1Down-RegulationGene ExpressionInterferon-gammaInterleukin-12Interleukin-17Lymph NodesMacrophagesMiceMice, Inbred C57BLAntibodies, Monoclonalaryl hydrocarbon receptor, XenopusBasic Helix-Loop-Helix ProteinsBlood GlucoseIl12rb1 protein, mouseIl12rb2 protein, mouseInterferon-gammaInterleukin-12Interleukin-17interleukin-23 receptor, mouseNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Aryl HydrocarbonReceptors, InterleukinReceptors, Interleukin-12Rorc protein, mouseT-Box Domain ProteinsXenopus Proteins

Identifiers

PMID19188681
PMCPMC2648686
OpenAlexW2072449713

What OpenQuestion holds

Textmetadata
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.