Evidence map›Paper›PMID 7908321›Full record

ArticleThe Journal of experimental medicine1994

In vivo priming of two distinct antitumor effector populations: the role of MHC class I expression.

H I Levitsky, A Lazenby, R J Hayashi, D M Pardoll

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 191 citations in OpenAlex.

  1. Article
  2. MHC class Ib-restricted CD8Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Review
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  17. Tumor-specific CD4+ melanoma tumor-infiltrating lymphocytes.Journal of immunotherapy (Hagerstown, Md. : 1997) · 2012
    Article
  18. Review
  19. Article
  20. Combination approaches to potentiate immune response after photodynamic therapy for cancer.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2011
    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

4 authors at 1 institution in 1 country.

H I LevitskyDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
A Lazenby
R J Hayashi
D M Pardoll
Johns Hopkins University · US

Funding

NOVEL T CELL SUBSET--NK1+ ALPHA BETAK08CA001595 · NCI · JOHNS HOPKINS UNIVERSITY · PI LEVITSKY, HYAM ISAAC · 1991 to 1995
–
MECHANISMS OF IMMUNITY TO TUMOR ANTIGENSR01CA057842 · NCI · JOHNS HOPKINS UNIVERSITY · PI PARDOLL, DREW M. · 1992 to 1999
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NCI NIH HHS 1R01CA57842-01NCI NIH HHS SK08CA01595-02
6 · The paper itself

Abstract

Downregulation of major histocompatibility complex (MHC) class I expression is an important mechanism by which tumors evade classical T cell-dependent immune responses. Therefore, a system was designed to evaluate parameters for active immunization against MHC class I- tumors. Mice were capable of rejecting a MHC class I- tumor challenge after immunization with an irradiated granulocyte/macrophage colony-stimulating factor (GM-CSF) transduced MHC class I- tumor vaccine. This response was critically dependent on CD4+ T cells and natural killer (NK) cells, but minimally on CD8+ T cells. A strong protective response against MHC class I+ variants of the tumor could be elicited when mice were immunized with irradiated MHC class I+ GM-CSF-secreting tumor cells. This response required CD4+ and CD8+ T cells, and in addition, elimination of NK cells resulted in outgrowth of tumors that had lost expression of at least one MHC class I gene. Finally, class I MHC expression on the vaccinating cells inhibited the response generated against a MHC class I- tumor challenge. These results demonstrate that the host is capable of being immunized against a tumor that has lost MHC class I expression and reveal conditions under which distinct effector cells play a role in the systemic antitumor immune response.

Indexed as

AnimalsBase SequenceCD4-Positive T-LymphocytesDNADown-RegulationGranulocyte-Macrophage Colony-Stimulating FactorHistocompatibility Antigens Class IMiceMice, Inbred BALB CMice, Inbred C57BLMolecular Sequence DataNeoplasms, ExperimentalNeoplasm TransplantationT-LymphocytesT-Lymphocytes, RegulatoryTransduction, GeneticDNAGranulocyte-Macrophage Colony-Stimulating FactorHistocompatibility Antigens Class I

Identifiers

PMID7908321
PMCPMC2191440
OpenAlexW2149366474

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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 OpenQuestion graph.