Evidence map›Paper›PMID 20349123›Full record

ArticleJournal of clinical immunology2010

TL1A selectively enhances IL-12/IL-18-induced NK cell cytotoxicity against NK-resistant tumor targets.

Stephanie C Heidemann, Valerie Chavez, Carol J Landers, Torsten Kucharzik, John L Prehn, Stephan R Targan

Open access · hybridAbstract read
In one paragraph

Article in Journal of clinical immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  6. Review
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  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Immunobiology of TNFSF15 and TNFRSF25.Immunologic research · 2013
    Review
  16. Article
  17. Article
  18. Review
  19. TNFSF15 Modulates Neovascularization and Inflammation.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012
    Article
  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

6 authors at 2 institutions in 2 countries.

Stephanie C HeidemannInflammatory Bowel Disease Research Center, Cedars-Sinai Medical Center, 8700 Beverly Blvd., D4063, Los Angeles, CA, 90048, USA.
Valerie Chavez
Carol J Landers
Torsten Kucharzik
John L Prehn
Stephan R Targan
Cedars-Sinai Medical Center · USUniversity of Münster · DE

Funding

Using polygenic scores to enhance both variant discovery, and understanding of functional consequences of genetic variation in IBD.P01DK046763 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1992 to 2020
$31.1M
TNF ALPHA AND CROHNS DISEASE MUCOSAL INFLAMMATIONR01DK056328 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1999 to 2018
$6.9M
NIDDK NIH HHS DK056328NIDDK NIH HHS P01 DK046763NIDDK NIH HHS R01 DK056328
6 · The paper itself

Abstract

introductionTL1A (TNFSF15) augments IFN-gamma production by IL-12/IL-18 responsive human T cells. Its ligand, death domain receptor 3 (DR3), is induced by activation on T and NK cells. Although IL-12/IL-18 induces DR3 expression on most NK cells, addition of TL1A minimally increases IFN-gamma production.

methods(51)Chromium release and flow cytometric analysis were used to determine whether the TL1A-DR3 pathway is implicated in tumor cell lysis. Our aim was to determine whether the TL1A-DR3 pathway is implicated in tumor cell lysis.

resultsTL1A had no additional effect on IL-12/IL-18-induced cytotoxicity against an NK-susceptible tumor (K562); however, it promoted cytotoxicity against NK-resistant targets susceptible to lysis only by activated NK cells. DISCUSSION: With IL-12/IL-18 activation, TL1A increased CD107a expression on NK cells which led to enhanced lysis of Daudi by PBMC and purified NK cells. To a lesser degree, TL1A increased lysis of colorectal adenocarcinoma epithelial derived lines (WiDr and SW837) by IL-12/IL-18-activated cells.

conclusionTL1A increased cytotoxicity of IL-12/IL-18-activated NK cells against target cells dependent on NK activation for lysis and could function in vivo as a key co-activator of NK cytotoxicity.

Indexed as

Cell Line, TumorCytotoxicity, ImmunologicHumansInterleukin-12Interleukin-18Killer Cells, NaturalLysosomal-Associated Membrane Protein 1NeoplasmsReceptors, Tumor Necrosis Factor, Member 25Tumor Necrosis Factor Ligand Superfamily Member 15Interleukin-12Interleukin-18Lysosomal-Associated Membrane Protein 1Receptors, Tumor Necrosis Factor, Member 25TNFSF15 protein, humanTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID20349123
PMCPMC2900590
OpenAlexW2015477536

What OpenQuestion holds

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LicenceCC BY-NC
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.