Evidence map›Paper›PMID 40660233›Full record

ArticleJournal of translational medicine2025

Abnormal metabolic activation of CD8

Bixia Wang, Jianing Tang, Yang Zhou, Qianqian Huang, Xinya Jiang, Fangqing Zhang, Shuang Fan, Qi Zhang, Jingrui Zhou, Yu Wang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

12 authors.

Bixia Wang *Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Jianing Tang *Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Yang ZhouPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Qianqian HuangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Xinya JiangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Fangqing ZhangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Shuang FanPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Qi ZhangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Jingrui ZhouPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Yu WangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Xiao-Jun HuangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China.
Huidong GuoPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Peking University, No 11, Xizhimen South Street, Beijing, 100044, China. guohuidong@bjmu.edu.cn.

Funding

Beijing Municipal Health Commission project BRWEP2024W134080115Beijing Natural Science Foundation General Project 7252142Major Program of the National Natural Science Foundation of China 82293630National Natural Science Foundation of China 82300243
6 · The paper itself

Abstract

backgroundAllogeneic hematopoietic stem cell transplantation (allo-HSCT) is a critical therapeutic strategy for acute myeloid leukemia (AML). However, relapse remains a major challenge, with limited effective options for managing post-transplant recurrence. Tumor cells escape immune surveillance by establishing a complex, immunosuppressive tumor microenvironment (TME), which plays a central role in immune evasion and disease relapse. Understanding the TME’s impact on immune cells and their functional alterations is therefore of significant clinical importance.

methodsUtilizing a non-irradiated AML mouse model and bioinformatic analysis, we systematically analyzed T-cell dynamics during AML progression and identified abnormal metabolic activation in CD8+ T cells at early disease stages, which correlated with leukemia cell immune evasion.

resultWe found that when major histocompatibility complex (MHC) molecules on AML cells were haplomatched with immune cells, CD8+ T cells exhibited robust cytokine and cytotoxic activation, retaining immune profiles similar to those of normal T cells. However, under the same tumor burden, T cells, particularly CD8+ T cells, showed dramatic metabolic gene activation in MHC-matched leukemic mice. This metabolic activation led to rapid exhaustion of CD8+ T cells, accelerating leukemia progression. Based on these activated metabolic genes, we established a metabolism-associated genes (MAGs) scoring system. Validation using public datasets revealed that a high MAG score is associated with poor prognosis in AML patients.

conclusionsOur findings provide molecular evidence supporting the stronger graft-versus-leukemia effects observed in HLA haploidentical HSCT. Moreover, they highlight that abnormal metabolic activation in CD8+ T cells during early AML progression contributes to rapid disease advancement and poor prognosis.

Indexed as

CD8-Positive T-LymphocytesLeukemia, Myeloid, AcuteAnimalsHumansLymphocyte ActivationMiceMice, Inbred C57BLPrognosisTumor Microenvironment

Identifiers

PMID40660233
PMCPMC12257688

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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 OpenQuestion graph.