Evidence map›Paper›PMID 32622347›Full record

ReviewInternational immunology2021

Immune metabolism in PD-1 blockade-based cancer immunotherapy.

Alok Kumar, Kenji Chamoto

Open access · bronzeAbstract readReview
In one paragraph

Review in International immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 11% of its field
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

26 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  4. Article
  5. Adoptive T-Cell Therapy in Sarcomas.Current oncology reports · 2025
    Review
  6. Mitochondrial Metabolism in T-Cell Exhaustion.International journal of molecular sciences · 2025
    Review
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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

2 authors at 1 institution in 1 country.

Alok KumarDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida, Konoe-cho, Sakyo-ku, Kyoto, Japan.
Kenji ChamotoDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida, Konoe-cho, Sakyo-ku, Kyoto, Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Energy metabolism plays an important role in proliferating cells. Recent reports indicate that metabolic regulation or metabolic products can control immune cell differentiation, fate and reactions. Cancer immunotherapy based on blockade of programmed cell death protein 1 (PD-1) has been used worldwide, but a significant fraction of patients remain unresponsive. Therefore, clarifying the mechanisms and overcoming the unresponsiveness are urgent issues. Because cancer immunity consists of interactions between the cancer and host immune cells, there has recently been a focus on the metabolic interactions and/or competition between the tumor and the immune system to address these issues. Cancer cells render their microenvironment immunosuppressive, driving T-cell dysfunction or exhaustion, which is advantageous for cancer cell survival. However, accumulating mechanistic evidence of T-cell and cancer cell metabolism has gradually revealed that controlling the metabolic pathways of either type of cell can overcome T-cell dysfunction and reprogram the metabolic balance in the tumor microenvironment. Here, we summarize the role of immune metabolism in T-cell-based immune surveillance and cancer immune escape. This new concept has boosted the development of combination therapy and predictive biomarkers in cancer immunotherapy with immune checkpoint inhibitors.

Indexed as

Cell DifferentiationCombined Modality TherapyEnergy MetabolismHumansImmune Checkpoint InhibitorsImmunotherapyNeoplasmsProgrammed Cell Death 1 ReceptorT-LymphocytesTumor EscapeTumor MicroenvironmentImmune Checkpoint InhibitorsPDCD1 protein, humanProgrammed Cell Death 1 Receptorbiomarkercombination therapyenergy metabolismimmune checkpointmitochondria

Identifiers

PMID32622347
PMCPMC7771015
OpenAlexW3039388108

What OpenQuestion holds

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LicenceCC BY-NC
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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.