Evidence map›Paper›PMID 41673089›Full record

ArticleScientific reports2026

Targeting of specific neuronal types in the non-human primate brain by using a murine CD25-specific recombinant immunotoxin.

Tomoko Kobayashi, Shigeki Kato, Shingo Kimura, Masateru Sugawara, Kanichiro Ihara, Tatsuhiko Ozawa, Ken-Ichi Inoue, Masahiko Takada, Masanori Onda, Kazuto Kobayashi

Abstract read
In one paragraph

Article in Scientific reports, 2026. 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

10 authors.

Tomoko KobayashiDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan.
Shigeki KatoDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan.
Shingo KimuraDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan.
Masateru SugawaraDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan.
Kanichiro IharaDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan.
Tatsuhiko OzawaDepartment of Life Sciences and Bioengineering, Laboratory of Molecular and Cellular Biology, Faculty of Engineering, Academic Assembly, University of Toyama, Toyama, 930-8555, Japan.
Ken-Ichi InoueCenter for the Evolutionary Origins of Human Behavior, Kyoto University, Inuyama, Aichi, 484-8506, Japan.
Masahiko TakadaCenter for the Evolutionary Origins of Human Behavior, Kyoto University, Inuyama, Aichi, 484-8506, Japan.
Masanori OndaLaboratory of Molecular Biology, National Cancer Institutes, National Institutes of Health, Bethesda, 20892, USA.
Kazuto KobayashiDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan. kazuto@fmu.ac.jp.

Funding

Japan Agency for Medical Research and Development 25wm0625103h0002Japan Agency for Medical Research and Development JP21am0101077Ministry of Education, Science, Sports, and Culture of Japan 21H05244
6 · The paper itself

Abstract

Immunotoxin (ITX)-mediated cell targeting enables selective elimination of neuronal types of interest from a complex neural network. In this technology, human interleukin-2 receptor α-subunit or CD25 (hCD25) is expressed in specific cell types in transgenic rodents, and then the animals are treated with a recombinant ITX composed of monoclonal antibody variable regions for hCD25 fused to a Pseudomonas exotoxin fragment (PE38), resulting in the ablation of hCD25-expressing cells. However, there is a critical issue on the cross-reactivity of the recombinant ITX for endogenous CD25 in non-human primates (NHPs), leading to off-target effects. Here we generated a mouse CD25 (mCD25)-specific recombinant ITX, termed anti-mCD25-PE38, based on variable regions of a rabbit monoclonal antibody that specifically reacts to mCD25, but not to hCD25. Anti-mCD25-PE38 showed high-affinity binding to mCD25 and cytotoxic activity toward mCD25-expressing cells. Injection of anti-mCD25-PE38 into the ventral midbrain of common marmosets, in which the mCD25 transgene was expressed in dopamine neurons by a lentiviral vector for retrograde gene transfer, induced a significant loss of midbrain dopamine neurons. Therefore, anti-mCD25-PE38 provides a useful strategy for selective targeting of neuronal types to study the behavioral and neurological functions of these neurons in the NHP brain.

Indexed as

BrainImmunotoxinsInterleukin-2 Receptor alpha SubunitNeuronsAnimalsAntibodies, MonoclonalCallithrixExotoxinsHumansMiceRecombinant ProteinsAntibodies, MonoclonalExotoxinsImmunotoxinsInterleukin-2 Receptor alpha SubunitRecombinant Proteins

Identifiers

PMID41673089
PMCPMC12963413

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LicenceCC BY-NC-ND
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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.