Evidence map›Paper›PMID 19654865›Full record

ArticlePloS one2009

Abnormally high levels of virus-infected IFN-gamma+ CCR4+ CD4+ CD25+ T cells in a retrovirus-associated neuroinflammatory disorder.

Yoshihisa Yamano, Natsumi Araya, Tomoo Sato, Atae Utsunomiya, Kazuko Azakami, Daisuke Hasegawa, Toshihiko Izumi, Hidetoshi Fujita, Satoko Aratani, Naoko Yagishita and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

77 citing papers in PubMed, 129 citations in OpenAlex.

  1. Trial
  2. Clinical trial of raltegravir, an integrase inhibitor, in HAM/TSP.Annals of clinical and translational neurology · 2021
    Trial
  3. Article
  4. Loss of HTLV-1-specific CD8Blood neoplasia · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Complete Rescue of HTLV-1Pathogens (Basel, Switzerland) · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

17 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 2 countries.

Yoshihisa YamanoDepartment of Molecular Medical Science, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan. yyamano@marianna-u.ac.jp
Natsumi Araya
Tomoo Sato
Atae Utsunomiya
Kazuko Azakami
Daisuke Hasegawa
Toshihiko Izumi
Hidetoshi Fujita
Satoko Aratani
Naoko Yagishita
Ryoji Fujii
Kusuki Nishioka
Steven Jacobson
Toshihiro Nakajima
St. Marianna University School of Medicine · JPImamura Hospital · JPNational Institutes of Health · US

Funding

Involvement Of Human Viruses Associated With Chronic Neurologic DiseaseZIANS002817 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI JACOBSON, STEVEN · 2009 to 2025
$26.5M
Retrovirus Associated With Chronic Neurologic DiseaseZ01NS002817 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI JACOBSON, STEVEN · 1990 to 2008
$4.0M
6 · The paper itself

Abstract

backgroundHuman T-lymphotropic virus type 1 (HTLV-1) is a human retrovirus associated with both HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), which is a chronic neuroinflammatory disease, and adult T-cell leukemia (ATL). The pathogenesis of HAM/TSP is known to be as follows: HTLV-1-infected T cells trigger a hyperimmune response leading to neuroinflammation. However, the HTLV-1-infected T cell subset that plays a major role in the accelerated immune response has not yet been identified. PRINCIPAL

findingsHere, we demonstrate that CD4(+)CD25(+)CCR4(+) T cells are the predominant viral reservoir, and their levels are increased in HAM/TSP patients. While CCR4 is known to be selectively expressed on T helper type 2 (Th2), Th17, and regulatory T (Treg) cells in healthy individuals, we demonstrate that IFN-gamma production is extraordinarily increased and IL-4, IL-10, IL-17, and Foxp3 expression is decreased in the CD4(+)CD25(+)CCR4(+) T cells of HAM/TSP patients as compared to those in healthy individuals, and the alteration in function is specific to this cell subtype. Notably, the frequency of IFN-gamma-producing CD4(+)CD25(+)CCR4(+)Foxp3(-) T cells is dramatically increased in HAM/TSP patients, and this was found to be correlated with disease activity and severity.

conclusionsWe have defined a unique T cell subset--IFN-gamma(+)CCR4(+)CD4(+)CD25(+) T cells--that is abnormally increased and functionally altered in this retrovirus-associated inflammatory disorder of the central nervous system.

Indexed as

Case-Control StudiesCD4 AntigensCell ProliferationHTLV-I InfectionsHuman T-lymphotropic virus 1Interferon-gammaInterleukin-10Interleukin-2 Receptor alpha SubunitInterleukin-4Nervous System DiseasesReceptors, CCR4T-LymphocytesCD4 AntigensInterferon-gammaInterleukin-10Interleukin-2 Receptor alpha SubunitInterleukin-4Receptors, CCR4

Identifiers

PMID19654865
PMCPMC2715877
OpenAlexW2123524329

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.