Evidence map›Paper›PMID 26903482›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Cutting Edge: Engineering Active IKKβ in T Cells Drives Tumor Rejection.

César Evaristo, Stefani Spranger, Sarah E Barnes, Michelle L Miller, Luciana L Molinero, Frederick L Locke, Thomas F Gajewski, Maria-Luisa Alegre

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

24 citing papers in PubMed, 28 citations in OpenAlex.

  1. Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
  2. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  3. Review
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  5. Review
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  7. Bioinformatic Analysis ofInternational journal of molecular sciences · 2024
    Article
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  20. Hsp90 Interacts with the Bacterial Effector NleH1.Pathogens (Basel, Switzerland) · 2018
    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

8 authors at 1 institution in 1 country.

César EvaristoDepartment of Medicine, University of Chicago, Chicago, IL 60637; and.ORCID http://orcid.org/0000-0002-2281-1045
Stefani SprangerDepartment of Pathology, University of Chicago, Chicago, IL 60637.ORCID http://orcid.org/0000-0003-3257-4546
Sarah E BarnesDepartment of Medicine, University of Chicago, Chicago, IL 60637; and.ORCID http://orcid.org/0000-0001-5047-2549
Michelle L MillerDepartment of Medicine, University of Chicago, Chicago, IL 60637; and.
Luciana L MolineroDepartment of Medicine, University of Chicago, Chicago, IL 60637; and.ORCID http://orcid.org/0000-0001-5866-5214
Frederick L LockeDepartment of Medicine, University of Chicago, Chicago, IL 60637; and.ORCID http://orcid.org/0000-0001-9063-6691
Thomas F GajewskiDepartment of Medicine, University of Chicago, Chicago, IL 60637; and Department of Pathology, University of Chicago, Chicago, IL 60637.
Maria-Luisa AlegreDepartment of Medicine, University of Chicago, Chicago, IL 60637; and malegre@midway.uchicago.edu.
University of Chicago · US

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI MARK W. LINGEN · 1985 to 2026
$122.1M
Role of NF-kB Activation in Acute Allograft RejectionR01AI052352 · NIAID · UNIVERSITY OF CHICAGO · PI ALEGRE, MARIA-LUISA · 2004 to 2014
$3.4M
T Cell Responsiveness and Homeostasis in Anti-TumorR01CA118153 · NCI · UNIVERSITY OF CHICAGO · PI GAJEWSKI, THOMAS F · 2006 to 2010
$1.3M
NCI NIH HHS P30 CA014599NCI NIH HHS R01 CA118153NCI NIH HHS R01CA118153NIAID NIH HHS R01 AI052352PHS HHS 5 P30 CAO14599-35
6 · The paper itself

Abstract

Acquired dysfunction of tumor-reactive T cells is one mechanism by which tumors can evade the immune system. Identifying and correcting pathways that contribute to such dysfunction should enable novel anticancer therapy design. During cancer growth, T cells show reduced NF-κB activity, which is required for tumor rejection. Impaired T cell-intrinsic NF-κB may create a vicious cycle conducive to tumor progression and further T cell dysfunction. We hypothesized that forcing T cell-intrinsic NF-κB activation might break this cycle and induce tumor elimination. NF-κB was activated in T cells by inducing the expression of a constitutively active form of the upstream activator IκB kinase β (IKKβ). T cell-restricted constitutively active IKKβ augmented the frequency of functional tumor-specific CD8(+) T cells and improved tumor control. Transfer of constitutively active IKKβ-transduced T cells also boosted endogenous T cell responses that controlled pre-established tumors. Our results demonstrate that driving T cell-intrinsic NF-κB can result in tumor control, thus identifying a pathway with potential clinical applicability.

Indexed as

Genetic EngineeringAdoptive TransferAnimalsCD8-Positive T-LymphocytesCell Line, TumorCytotoxicity, ImmunologicDisease Models, AnimalGene ExpressionHeterograftsHumansI-kappa B KinaseInterferon-gammaLymphocyte CountLymphocytes, Tumor-InfiltratingMiceMice, TransgenicI-kappa B KinaseInterferon-gammaNF-kappa B

Identifiers

PMID26903482
PMCPMC4799771
OpenAlexW2307462615

What OpenQuestion holds

Textmetadata
LicenceTDM
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.