Evidence map›Paper›PMID 25340344›Full record

ArticlePLoS pathogens2014

A critical role for IL-17RB signaling in HTLV-1 tax-induced NF-κB activation and T-cell transformation.

Alfonso Lavorgna, Masao Matsuoka, Edward William Harhaj

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The World according to IL-9.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Targeting the IL-9 pathway in cancer immunotherapy.Human vaccines & immunotherapeutics · 2020
    Review
  14. The Role of Interleukin-9 in Cancer.Pathology oncology research : POR · 2020
    Review
  15. Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

3 authors at 2 institutions in 2 countries.

Alfonso LavorgnaDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America.
Masao MatsuokaLaboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Edward William HarhajDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America.
Sidney Kimmel Comprehensive Cancer Center · USKyoto University · JP

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Mechanisms of HTLV-I Tax-mediated NF-kB activationR01CA135362 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARHAJ, EDWARD W · 2009 to 2018
$2.7M
NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA135362NCI NIH HHS R01CA135362
6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) infection is linked to the development of adult T-cell leukemia (ATL) and the neuroinflammatory disease HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax protein functions as a potent viral oncogene that constitutively activates the NF-κB transcription factor to transform T cells; however, the underlying mechanisms remain obscure. Here, using next-generation RNA sequencing we identified the IL-25 receptor subunit IL-17RB as an aberrantly overexpressed gene in HTLV-1 immortalized T cells. Tax induced the expression of IL-17RB in an IκB kinase (IKK) and NF-κB-dependent manner. Remarkably, Tax activation of the canonical NF-κB pathway in T cells was critically dependent on IL-17RB expression. IL-17RB and IL-25 were required for HTLV-1-induced immortalization of primary T cells, and the constitutive NF-κB activation and survival of HTLV-1 transformed T cells. IL-9 was identified as an important downstream target gene of the IL-17RB pathway that drives the proliferation of HTLV-1 transformed cells. Furthermore, IL-17RB was overexpressed in leukemic cells from a subset of ATL patients and also regulated NF-κB activation in some, but not all, Tax-negative ATL cell lines. Together, our results support a model whereby Tax instigates an IL-17RB-NF-κB feed-forward autocrine loop that is obligatory for HTLV-1 leukemogenesis.

Indexed as

Signal TransductionCell Transformation, NeoplasticGene Expression RegulationGene Products, taxHumansHuman T-lymphotropic virus 1Interleukin-17NF-kappa BReceptors, Interleukin-17T-LymphocytesGene Products, taxIL17A protein, humanInterleukin-17NF-kappa BReceptors, Interleukin-17tax protein, Human T-lymphotrophic virus 1

Identifiers

PMID25340344
PMCPMC4207800
OpenAlexW2023993028

What OpenQuestion holds

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Read underepoch 390

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.