Evidence map›Paper›PMID 10510086›Full record

ArticleThe Journal of experimental medicine1999

A defect in interleukin 12-induced activation and interferon gamma secretion of peripheral natural killer T cells in nonobese diabetic mice suggests new pathogenic mechanisms for insulin-dependent diabetes mellitus.

M Falcone, B Yeung, L Tucker, E Rodriguez, N Sarvetnick

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.6field-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

36 citing papers in PubMed, 134 citations in OpenAlex.

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  13. Elimination of insulitis and augmentation of islet beta cell regeneration via induction of chimerism in overtly diabetic NOD mice.Proceedings of the National Academy of Sciences of the United States of America · 2007
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  18. Mouse V alpha 14i natural killer T cells are resistant to cytokine polarization in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2003
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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

5 authors at 2 institutions in 2 countries.

M FalconeDepartment of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA.
B Yeung
L Tucker
E Rodriguez
N Sarvetnick
Scripps Research Institute · USNHS Blood and Transplant · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The function of natural killer T (NKT) cells in the immune system has yet to be determined. There is some evidence that their defect is associated with autoimmunity, but it is still unclear how they play a role in regulating the pathogenesis of T cell-mediated autoimmune diseases. It was originally proposed that NKT cells could control autoimmunity by shifting the cytokine profile of autoimmune T cells toward a protective T helper 2 cell (Th2) type. However, it is now clear that the major function of NKT cells in the immune system is not related to their interleukin (IL)-4 secretion. In fact, NKT cells mainly secrete interferon (IFN)-gamma and, activated in the presence of IL-12, acquire a strong inflammatory phenotype and cytotoxic function.

Indexed as

AnimalsAutoimmunityCell DifferentiationDiabetes Mellitus, Type 1InflammationInterferon-gammaInterleukin-12Killer Cells, NaturalLymphocyte ActivationMiceMice, Inbred C57BLMice, Inbred NODMice, SCIDPhenotypeReceptors, Antigen, T-CellTh2 CellsInterferon-gammaInterleukin-12Receptors, Antigen, T-Cell

Identifiers

PMID10510086
PMCPMC2195642
OpenAlexW2074843663

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.