Evidence map›Paper›PMID 40046256›Full record

ArticleBiochemistry and biophysics reports2025

MHC class I trafficking signal improves induction of cytotoxic T lymphocyte using artificial antigen presenting cells.

Kenta Sasaki, Kenji Murata, Tomoyuki Minowa, Naoki Shijubou, Hiroki Kobayashi, Munehide Nakatsugawa, Aiko Murai, Yuka Mizue, Terufumi Kubo, Takayuki Kanaseki and 5 more

Abstract read
In one paragraph

Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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

15 authors.

Kenta SasakiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Kenji MurataDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Tomoyuki MinowaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Naoki ShijubouDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Hiroki KobayashiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Munehide NakatsugawaDepartment of Pathology, Tokyo Medical University Hachioji Medical Center, Hachioji, Tokyo, 193-0998, Japan.
Aiko MuraiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Yuka MizueDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Terufumi KuboDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Takayuki KanasekiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Tomohide TsukaharaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Hisashi UharaDepartment of Dermatology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Akemi Ishida-YamamotoDepartment of Dermatology, Asahikawa Medical University School of Medicine, Asahikawa, Hokkaido, 078-8510, Japan.
Yoshihiko HirohashiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.
Toshihiko TorigoeDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, 060-8556, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inducing antigen peptide-specific cytotoxic T cells is challenging, partly due to the difficulty of maintaining the quality of antigen-presenting cells, such as dendritic cells. Consequently, artificial antigen-presenting cells (aAPCs) derived from the erythroleukemia cell line K562 have been employed for T cell stimulation. K562-based aAPCs can be utilized for both non-specific and antigen-specific T cell stimulation. Antigen peptide-pulsed aAPCs are commonly used to stimulate T cells with known specific antigenic peptides, which require identifying antigenic peptides from cognate antigen proteins. Therefore, antigen gene-overexpressing aAPCs might be useful for detecting unknown antigenic peptides. In this study, we evaluated the efficacy of cytotoxic T lymphocyte (CTL) induction using antigen gene-overexpressing aAPCs. To enhance antigen presentation efficiency, we assessed the signal peptide (SP) fused with MHC class I trafficking signal (MITD) sequences (SP-MITD). SP-MITD, fused with epitopes from the neoantigen AKF9 and the viral antigen CMVpp65, was transduced into aAPCs. We compared the CTL induction ability of peptide-pulsed aAPCs, only mini-gene-overexpressing aAPCs [SP-MITD (-)], and mini-gene fused with SP-MITD overexpressing aAPCs [SP-MITD (+)]. The SP-MITD (+) gene-overexpressing aAPCs exhibited the highest CTL induction efficiency compared to both peptide-pulsed and SP-MITD (-) gene-overexpressing aAPCs. These findings suggest that antigen gene-fused with SP-MITD transduced aAPCs are highly effective for inducing CTLs specific to both known and unknown antigenic peptides.

Indexed as

Artificial antigen-presenting cells (aAPC)Erythroleukemia cell line K562MHC class I trafficking signal (MITD)

Identifiers

PMID40046256
PMCPMC11880709

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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.