Evidence map›Paper›PMID 39106105›Full record

ArticleJCI insight2024

Pharmacological induction of MHC-I expression in tumor cells revitalizes T cell antitumor immunity.

Qian Yu, Yu Dong, Xiaobo Wang, Chenxuan Su, Runkai Zhang, Wei Xu, Shuai Jiang, Yongjun Dang, Wei Jiang

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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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

9 authors.

Qian YuKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, and.
Yu DongDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaobo WangKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, and.
Chenxuan SuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.
Runkai ZhangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.
Wei XuInstitute of Immunological Innovation and Translation and.
Shuai JiangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yongjun DangBasic Medicine Research and Innovation Center for Novel Target and Therapeutic Intervention, Ministry of Education, College of Pharmacy, Chongqing Medical University, Chongqing Medical University, Chongqing, China.
Wei JiangKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, and.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antigen presentation by major histocompatibility complex class I (MHC-I) is crucial for T cell-mediated killing, and aberrant surface MHC-I expression is tightly associated with immune evasion. To address MHC-I downregulation, we conducted a high-throughput flow cytometry screen, identifying bleomycin (BLM) as a potent inducer of cell surface MHC-I expression. BLM-induced MHC-I augmentation rendered tumor cells more susceptible to T cells in coculture assays and enhanced antitumor responses in an adoptive cellular transfer mouse model. Mechanistically, BLM remodeled the tumor immune microenvironment, inducing MHC-I expression in a manner dependent on ataxia-telangiectasia mutated/ataxia telangiectasia and Rad3-related-NF-κB. Furthermore, BLM improved T cell-dependent immunotherapeutic approaches, including bispecific antibody therapy, immune checkpoint therapy, and autologous tumor-infiltrating lymphocyte therapy. Importantly, low-dose BLM treatment in mouse models amplified the antitumor effect of immunotherapy without detectable pulmonary toxicity. In summary, our findings repurpose BLM as a potential inducer of MHC-I, enhancing its expression to improve the efficacy of T cell-based immunotherapy.

Indexed as

BleomycinHistocompatibility Antigens Class IT-LymphocytesTumor MicroenvironmentAnimalsCell Line, TumorFemaleHumansImmunotherapyMiceMice, Inbred C57BLNeoplasmsBleomycinHistocompatibility Antigens Class ICancer immunotherapyDrug screensMHC class 1Oncology

Identifiers

PMID39106105
PMCPMC11385079

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.