Evidence map›Paper›PMID 41012676›Full record

ArticleViruses2025

An HTLV-1-Infected Humanized Mouse Model Expressing HLA-A*02:01 Demonstrates Effective CTL-Mediated Suppression of HTLV-1.

Shinsuke Nakajima, Motohito Goto, Sung-Il Lee, Tokifumi Odaka, Masaki Hino, Kenta Tezuka, Norihiro Takenouchi, Takaharu Ueno, Fhahira Rizkhika Admadiani, Riichi Takahashi and 4 more

Abstract read
In one paragraph

Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Shinsuke NakajimaDepartment of Microbiology, Faculty of Medicine, Kansai Medical University, Hirakata 573-1010, Japan.
Motohito GotoCentral Institute for Experimental Medicine and Life Science (CIEM), Kawasaki 210-0821, Japan.ORCID 0000-0001-6288-4583
Sung-Il LeeDepartment of Model Animal, Institute of Biomedical Science, Kansai Medical University, Hirakata 573-1010, Japan.ORCID 0000-0001-8330-1543
Tokifumi OdakaDepartment of Microbiology, Faculty of Medicine, Kansai Medical University, Hirakata 573-1010, Japan.
Masaki HinoDepartment of Microbiology, Faculty of Medicine, Kansai Medical University, Hirakata 573-1010, Japan.
Kenta TezukaCenter for Next Generation Biologics Research, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo 208-0011, Japan.
Norihiro TakenouchiDepartment of Microbiology, Faculty of Medicine, Kansai Medical University, Hirakata 573-1010, Japan.
Takaharu UenoDepartment of Microbiology, Faculty of Medicine, Kansai Medical University, Hirakata 573-1010, Japan.ORCID 0000-0002-4746-2726
Fhahira Rizkhika AdmadianiDepartment of Microbiology, Faculty of Medicine, Kansai Medical University, Hirakata 573-1010, Japan.
Riichi TakahashiCentral Institute for Experimental Medicine and Life Science (CIEM), Kawasaki 210-0821, Japan.ORCID 0000-0002-1930-7075
Isao HamaguchiCenter for Next Generation Biologics Research, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo 208-0011, Japan.
Takeshi TakahashiCentral Institute for Experimental Medicine and Life Science (CIEM), Kawasaki 210-0821, Japan.
Mamoru ItoCentral Institute for Experimental Medicine and Life Science (CIEM), Kawasaki 210-0821, Japan.ORCID 0000-0002-5373-8223
Kazu OkumaDepartment of Microbiology, Faculty of Medicine, Kansai Medical University, Hirakata 573-1010, Japan.ORCID 0009-0005-9719-0350

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) establishes lifelong infection and is associated with severe diseases such as adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Cytotoxic T lymphocytes (CTLs), especially those specific for the viral protein Tax, play a pivotal role in controlling HTLV-1 infection. However, conventional humanized mouse models fail to fully reconstitute human immune responses, limiting their utility for evaluating CTL-mediated immunity. This study aimed to establish a physiologically relevant in vivo model to investigate human CTL responses against HTLV-1. To achieve this, we utilized NOG-HLA-A02 transgenic (Tg) mice expressing human HLA-A02:01 on thymic epithelial cells, enabling proper development of HLA-restricted human T cells. Compared to conventional humanized NOG mice, HTLV-1-infected humanized NOG-HLA-A02 Tg mice exhibited significantly reduced HTLV-1 proviral load (PVL), decreased expansion of infected CD4

Indexed as

HLA-A2 AntigenHTLV-I InfectionsHuman T-lymphotropic virus 1T-Lymphocytes, CytotoxicAnimalsCD8-Positive T-LymphocytesDisease Models, AnimalGene Products, taxHumansMiceMice, TransgenicGene Products, taxHLA-A*02:01 antigenHLA-A2 AntigenHLAHTLV-1humanized mouseTax-specific CTLs

Identifiers

PMID41012676
PMCPMC12474424

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.