Evidence map›Paper›PMID 12941138›Full record

ArticleImmunology2003

Interleukin-12 and interleukin-2-induced invariant natural killer T-cell cytokine secretion and perforin expression independent of T-cell receptor activation.

Runhua Hou, Olga Goloubeva, Donna S Neuberg, Jack L Strominger, S Brian Wilson

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

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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 1 institution in 1 country.

Runhua HouDepartment of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
Olga Goloubeva
Donna S Neuberg
Jack L Strominger
S Brian Wilson
Dana-Farber Cancer Institute · US

Funding

Regulation of iNKT and APC InteractionsR01AI045051 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WILSON, S. BRIAN BRIAN · 1999 to 2009
$2.7M
NIAID NIH HHS R01 AI045051NIAID NIH HHS R01 AI45051
6 · The paper itself

Abstract

Human invariant natural killer (iNK) T cells expressing an invariant Valpha24-Jalpha15 T-cell receptor (TCR) are thought to be important regulators of autoimmunity and tumour surveillance. Two major subsets of iNK T cells, CD4+ or CD4- CD8- are known to exist, but the in vivo importance of CD4 expression is unclear. Since interleukin-12 (IL-12) is a key iNK T-cell-activating cytokine, the effect of IL-12 plus or minus the T-cell growth factor IL-2 on a large panel of CD4+ versus CD4- CD8- iNK T-cell clones was examined. Strikingly, IL-12 and IL-2 significantly activated iNK T cells to secrete IL-4, interferon-gamma and granulocyte-macrophage colony-stimulating factor, and up-regulated perforin expression in the absence of TCR stimulation. Furthermore, IL-2 and IL-12 treatment resulted in a preferential increase in apoptosis of CD4- CD8- clones. Thus, independent of TCR activation, IL-2 and IL-12 can directly activate iNK T cells and provide a selective advantage to the CD4+ iNK T-cell population.

Indexed as

ApoptosisCD4-Positive T-LymphocytesCells, CulturedCell SurvivalCytokinesHumansInterleukin-12Interleukin-2Killer Cells, NaturalLymphocyte ActivationMembrane GlycoproteinsPerforinPore Forming Cytotoxic ProteinsReceptors, Antigen, T-Cell, alpha-betaUp-RegulationCytokinesInterleukin-12Interleukin-2Membrane GlycoproteinsPerforinPore Forming Cytotoxic ProteinsReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID12941138
PMCPMC1783023
OpenAlexW1981137192

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.