Evidence map›Paper›PMID 8197161›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1994

The interleukin (IL) 2 receptor beta chain is shared by IL-2 and a cytokine, provisionally designated IL-T, that stimulates T-cell proliferation and the induction of lymphokine-activated killer cells.

R N Bamford, A J Grant, J D Burton, C Peters, G Kurys, C K Goldman, J Brennan, E Roessler, T A Waldmann

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01572493 (A Phase I Study of a Continuous Intravenous Infusion of Recombinant Human Interleukin IL-15), which is not on this map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
6.5field-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.

NCT01572493 phase1completednot on this mapstarted 2012, after this paper: background citation

A Phase I Study of a Continuous Intravenous Infusion of Recombinant Human Interleukin IL-15 (rhIL-15) in Adults With Metastatic Cancers

TypeinterventionalSponsorNational Cancer Institute (NCI)Ran2012 to 2019Enrolled38ConditionsLymphoma, CarcinomaArmsrh IL-15 (10 DAYS), rh IL-15 (5 DAYS)
3 · Its place in the literature

Who cites it

123 citing papers in PubMed, 412 citations in OpenAlex.

  1. Trial
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  3. TCF1bioRxiv : the preprint server for biology · 2026
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  14. Generation of Tumor-activated T cells Using Electroporation.Bioelectrochemistry (Amsterdam, Netherlands) · 2021
    Article
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  16. Review
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  20. Review

63 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

9 authors at 2 institutions in 1 country.

R N BamfordMetabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
A J Grant
J D Burton
C Peters
G Kurys
C K Goldman
J Brennan
E Roessler
T A Waldmann
National Cancer Institute · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Late-phase human T-cell lymphotropic virus I-associated adult T-cell leukemia cells express IL-2 receptors (IL-2R) but no longer produce IL-2. We have reported that the IL-2-independent adult T-cell leukemia line HuT-102 secretes a cytokine, provisionally designated IL-T, that stimulates T-cell proliferation and lymphokine-activated killer cell activity. Stimulation of proliferation of the cytokine-dependent human T-cell line Kit-225 mediated by HuT-102-conditioned medium or by 3200-fold-purified IL-T was not blocked by the addition of antibodies against IL-2 or IL-2R alpha subunit. However, IL-T-mediated stimulation of this human T-cell line was inhibited by addition of Mik-beta 1, an antibody that binds specifically to IL-2R beta subunit. In addition, the activation of large granular lymphocytes to lymphokine-activated killer cells mediated by IL-T-containing conditioned medium was not blocked by antibodies directed toward IL-2 or IL-2 alpha but was inhibited by an antibody to IL-2R beta, suggesting the requirement of this receptor subunit for IL-T action. This conclusion was confirmed using an IL-3-dependent murine myeloid precursor cell line, 32D, that expresses IL-2R alpha and IL-2R gamma, but not IL-2R beta. Neither IL-2 nor IL-T stimulated 32D cell proliferation. However, after transfection with the gene encoding human IL-2R beta, 32D beta cells proliferated on addition of either cytokine. The IL-T-mediated stimulation of 32D beta proliferation was inhibited by an anti-IL-2R beta antibody but not by an anti-IL-2 antibody. Thus, the IL-T-mediated stimulation of T-cell and lymphokine-activated killer cell activation requires the expression of the IL-2R beta subunit.

Indexed as

AnimalsAntibodies, MonoclonalCytotoxicity, ImmunologicHumansInterleukin-2Interleukin-3InterleukinsKiller Cells, Lymphokine-ActivatedLymphocyte ActivationMiceReceptors, Interleukin-2Signal TransductionT-LymphocytesTumor Cells, CulturedAntibodies, MonoclonalInterleukin-2Interleukin-3InterleukinsReceptors, Interleukin-2

Identifiers

PMID8197161
PMCPMC43905
OpenAlexW2018597572

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.