Evidence map›Paper›PMID 36283735›Full record

ArticleJournal for immunotherapy of cancer2022

Tumor MHC class I expression alters cancer-associated myelopoiesis driven by host NK cells.

Shi Yong Neo, Xu Jing, Le Tong, Dongmei Tong, Juan Gao, Ziqing Chen, Mireia Cruz De Los Santos, Nutsa Burduli, Sabrina De Souza Ferreira, Arnika Kathleen Wagner and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Natural killer cells drive 4-1BBL positive uveal melanoma towards EMT and metastatic disease.Journal of experimental & clinical cancer research : CR · 2024
    Article
  9. Review
  10. Review
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

14 authors at 5 institutions in 5 countries.

Shi Yong Neo *Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Xu Jing *Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Le TongDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Dongmei TongCentre for Innate Immunity and Infectious Disease, Hudson Institute of Medical Research, Melbourne, Victoria, Australia.
Juan GaoDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Ziqing ChenDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Mireia Cruz De Los SantosDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Nutsa BurduliDepartment of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
Sabrina De Souza FerreiraDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Arnika Kathleen WagnerDepartment of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
Evren AliciDepartment of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
Charlotte RolnyDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Yihai CaoDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Andreas LundqvistDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden Andreas.Lundqvist@ki.se.ORCID 0000-0002-9709-2970
Karolinska Institutet · SEAgency for Science, Technology and Research · SGHudson Institute of Medical Research · AUPrinceton University · USSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Downregulation of MHC class I (MHCI) molecules on tumor cells is recognized as a resistance mechanism of cancer immunotherapy. Given that MHCI molecules are potent regulators of immune responses, we postulated that the expression of MHCI by tumor cells influences systemic immune responses. Accordingly, mice-bearing MHCI-deficient tumor cells showed reduced tumor-associated extramedullary myelopoiesis in the spleen. Depletion of natural killer (NK) cells abrogated these differences, suggesting an integral role of immune-regulatory NK cells during tumor progression. Cytokine-profiling revealed an upregulation of TNF-α by NK cells in tumors and spleen in mice-bearing MHCI expressing tumors, and inhibition of TNF-α enhanced host myelopoiesis in mice receiving adoptive transfer of tumor-experienced NK cells. Our study highlights a critical role of NK cells beyond its identity as a killer lymphocyte and more importantly, the potential host responses to a localized tumor as determined by its MHCI expression.

Indexed as

MyelopoiesisNeoplasmsAnimalsHistocompatibility Antigens Class IKiller Cells, NaturalMiceTumor Necrosis Factor-alphaHistocompatibility Antigens Class ITumor Necrosis Factor-alphaAdaptive ImmunityKiller Cells, NaturalLymphocyte ActivationMyeloid-Derived Suppressor Cells

Identifiers

PMID36283735
PMCPMC9608525
OpenAlexW4307582136

What OpenQuestion holds

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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.