Evidence map›Paper›PMID 32471947›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

HTLV-1 induces T cell malignancy and inflammation by viral antisense factor-mediated modulation of the cytokine signaling.

Yusuke Higuchi, Jun-Ichirou Yasunaga, Yu Mitagami, Hirotake Tsukamoto, Kazutaka Nakashima, Koichi Ohshima, Masao Matsuoka

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Mouse Models for HTLV-1 Infection and Adult T Cell Leukemia.International journal of molecular sciences · 2023
    Review
  18. Review
  19. Article
  20. Review
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

7 authors at 3 institutions in 1 country.

Yusuke HiguchiLaboratory of Virus Control, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 606-8501, Japan.
Jun-Ichirou YasunagaLaboratory of Virus Control, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 606-8501, Japan; jyasunag@kumamoto-u.ac.jp.ORCID 0000-0002-7939-2080
Yu MitagamiLaboratory of Virus Control, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 606-8501, Japan.
Hirotake TsukamotoDepartment of Immunology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8555, Japan.ORCID 0000-0003-3214-1652
Kazutaka NakashimaDepartment of Pathology, School of Medicine, Kurume University, Kurume, Fukuoka 830-0011, Japan.
Koichi OhshimaDepartment of Pathology, School of Medicine, Kurume University, Kurume, Fukuoka 830-0011, Japan.ORCID 0000-0003-4996-5279
Masao MatsuokaLaboratory of Virus Control, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 606-8501, Japan.ORCID 0000-0002-0473-754X
Kyoto University · JPKurume University · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of a T cell neoplasm and several inflammatory diseases. A viral gene, HTLV-1 bZIP factor (HBZ), induces pathogenic Foxp3-expressing T cells and triggers systemic inflammation and T cell lymphoma in transgenic mice, indicating its significance in HTLV-1-associated diseases. Here we show that, unexpectedly, a proinflammatory cytokine, IL-6, counteracts HBZ-mediated pathogenesis. Loss of IL-6 accelerates inflammation and lymphomagenesis in HBZ transgenic mice. IL-6 innately inhibits regulatory T cell differentiation, suggesting that IL-6 functions as a suppressor against HBZ-associated complications. HBZ up-regulates expression of the immunosuppressive cytokine IL-10. IL-10 promotes T cell proliferation only in the presence of HBZ. As a mechanism of growth promotion by IL-10, HBZ interacts with STAT1 and STAT3 and modulates the IL-10/JAK/STAT signaling pathway. These findings suggest that HTLV-1 promotes the proliferation of infected T cells by hijacking the machinery of regulatory T cell differentiation. IL-10 induced by HBZ likely suppresses the host immune response and concurrently promotes the proliferation of HTLV-1 infected T cells.

Indexed as

AnimalsBasic-Leucine Zipper Transcription FactorsCell DifferentiationCell ProliferationHost-Pathogen InteractionsHTLV-I InfectionsHumansHuman T-lymphotropic virus 1Interleukin-10Interleukin-6LymphomaMiceMice, Inbred C57BLMice, KnockoutRetroviridae ProteinsT-Lymphocytes, RegulatoryBasic-Leucine Zipper Transcription FactorsHBZ protein, human T-cell leukemia virus type IInterleukin-10Interleukin-6Retroviridae ProteinsHBZHTLV-1IL-10IL-6JAK/STAT signaling pathway

Identifiers

PMID32471947
PMCPMC7306771
OpenAlexW3030715304

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.