Evidence map›Paper›PMID 26470881›Full record

ArticleBMC medical genomics2015

Gene expression profiling of the human natural killer cell response to Fc receptor activation: unique enhancement in the presence of interleukin-12.

Amanda R Campbell, Kelly Regan, Neela Bhave, Arka Pattanayak, Robin Parihar, Andrew R Stiff, Prashant Trikha, Steven D Scoville, Sandya Liyanarachchi, Sri Vidya Kondadasula and 4 more

Abstract read
In one paragraph

Article in BMC medical genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Trial
  2. Article
  3. PeerJ · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. EBI3 regulates the NK cell response to mouse cytomegalovirus infection.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  14. Article
  15. 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

14 authors.

Amanda R CampbellThe Arthur G. James Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH, 43210, USA. Amanda.Harper@osumc.edu.
Kelly ReganMedical Scientist Training Program and Biomedical Sciences Graduate Program, The Ohio State University, Columbus, OH, 43210, USA. Kelly.Regan@osumc.edu.
Neela BhaveThe Arthur G. James Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH, 43210, USA. Bhave.4@osu.edu.
Arka PattanayakDepartment of Biomedical Informatics, The Ohio State University, Columbus, OH, 43210, USA. Arka.Pattanayak@osumc.edu.
Robin PariharDepartment of Pediatrics, The Cleveland Clinic, Cleveland, OH, 44106, USA. rxpariha@txch.org.
Andrew R StiffThe Arthur G. James Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH, 43210, USA. Andrew.Stiff@osumc.edu.
Prashant TrikhaThe Arthur G. James Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH, 43210, USA. Prashant.Trikha@osumc.edu.
Steven D ScovilleThe Arthur G. James Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH, 43210, USA. Steven.Scoville@osumc.edu.
Sandya LiyanarachchiDivision of Human Cancer Genetics, The Ohio State University, Columbus, OH, 43210, USA. Sandya.Liyanarachchi@osumc.edu.
Sri Vidya KondadasulaDepartments of Oncology and Medicine, Wayne State University and Barbara Ann Karmanos Cancer Institute, Detroit, MI, 48201, USA. vidyakon@gmail.com.
Omkar LeleDepartment of Biomedical Informatics, The Ohio State University, Columbus, OH, 43210, USA. Omkar.Lele@osumc.edu.
Ramana DavuluriRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, 60611, USA. Ramana.Davuluri@northwestern.edu.
Philip R O PayneDepartment of Biomedical Informatics, The Ohio State University, Columbus, OH, 43210, USA. Philip.Payne@osumc.edu.
William E CarsonThe Arthur G. James Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH, 43210, USA. William.Carson@osumc.edu.

Funding

Northwestern University Clinical and Translational Science Institute (NUCATS)UL1TR001422 · NCATS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI D'AQUILA, RICHARD · 2015 to 2023
$56.8M
TWO SIGNAL REQUIREMENT FOR NATURAL KILLER IMMUNITYP01CA095426 · NCI · OHIO STATE UNIVERSITY · PI CALIGIURI, MICHAEL A · 2002 to 2016
$29.6M
The OSU Clinical and Translational Research Informatics Training Program (CTRIP)T15LM011270 · NLM · OHIO STATE UNIVERSITY · PI COOMBES, KEVIN ROBERT, JANIES, DANIEL A. · 2012 to 2016
$2.2M
The role of the aryl hydrocarbon receptor in natural killer cell development in normal and acute myeloid leukemia donorsF30CA196244 · NCI · OHIO STATE UNIVERSITY · PI SCOVILLE, STEVEN · 2015 to 2017
$129k
NCATS NIH HHS UL1 TR001422NCI NIH HHS F30 CA196244NCI NIH HHS P01 CA095426NCI NIH HHS P01 CA95426NLM NIH HHS 5T15LM011270-02NLM NIH HHS T15 LM011270
6 · The paper itself

Abstract

backgroundTraditionally, the CD56(dim)CD16(+) subset of Natural Killer (NK) cells has been thought to mediate cellular cytotoxicity with modest cytokine secretion capacity. However, studies have suggested that this subset may exert a more diverse array of immunological functions. There exists a lack of well-developed functional models to describe the behavior of activated NK cells, and the interactions between signaling pathways that facilitate effector functions are not well understood. In the present study, a combination of genome-wide microarray analyses and systems-level bioinformatics approaches were utilized to elucidate the transcriptional landscape of NK cells activated via interactions with antibody-coated targets in the presence of interleukin-12 (IL-12).

methodsWe conducted differential gene expression analysis of CD56(dim)CD16(+) NK cells following FcR stimulation in the presence or absence of IL-12. Next, we functionally characterized gene sets according to patterns of gene expression and validated representative genes using RT-PCR. IPA was utilized for biological pathway analysis, and an enriched network of interacting genes was generated using GeneMANIA. Furthermore, PAJEK and the HITS algorithm were employed to identify important genes in the network according to betweeness centrality, hub, and authority node metrics.

resultsAnalyses revealed that CD56(dim)CD16(+) NK cells co-stimulated via the Fc receptor (FcR) and IL-12R led to the expression of a unique set of genes, including genes encoding cytotoxicity receptors, apoptotic proteins, intracellular signaling molecules, and cytokines that may mediate enhanced cytotoxicity and interactions with other immune cells within inflammatory tissues. Network analyses identified a novel set of connected key players, BATF, IRF4, TBX21, and IFNG, within an integrated network composed of differentially expressed genes in NK cells stimulated by various conditions (immobilized IgG, IL-12, or the combination of IgG and IL-12).

conclusionsThese results are the first to address the global mechanisms by which NK cells mediate their biological functions when encountering antibody-coated targets within inflammatory sites. Moreover, this study has identified a set of high-priority targets for subsequent investigation into strategies to combat cancer by enhancing the anti-tumor activity of CD56(dim)CD16(+) NK cells.

Indexed as

Gene Regulatory NetworksGenomicsHumansImmunoglobulin GInterleukin-12Killer Cells, NaturalOligonucleotide Array Sequence AnalysisReceptors, FcTranscriptomeImmunoglobulin GInterleukin-12Receptors, Fc

Identifiers

PMID26470881
PMCPMC4608307

What OpenQuestion holds

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Registered trials

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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.