Evidence map›Paper›PMID 21969815›Full record

ArticleNeoplasia (New York, N.Y.)2011

Human leukocyte antigen E contributes to protect tumor cells from lysis by natural killer cells.

Elisa Lo Monaco, Elisa Tremante, Cristina Cerboni, Elisa Melucci, Leonardo Sibilio, Alessandra Zingoni, Maria Rita Nicotra, Pier Giorgio Natali, Patrizio Giacomini

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.5field-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

50 citing papers in PubMed, 90 citations in OpenAlex.

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  7. CD8Science advances · 2024
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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 at 2 institutions in 1 country.

Elisa Lo MonacoLaboratory of Immunology, Regina Elena Cancer Institute CRS, Rome, Italy.
Elisa Tremante
Cristina Cerboni
Elisa Melucci
Leonardo Sibilio
Alessandra Zingoni
Maria Rita Nicotra
Pier Giorgio Natali
Patrizio Giacomini
Sapienza University of Rome · ITConsorzio Interuniversitario Nazionale per la Bio-Oncologia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nonclassic class I human leukocyte antigen E (HLA-E) molecule engages the inhibitory NKG2A receptor on several cytotoxic effectors, including natural killer (NK) cells. Its tissue distribution was claimed to be wider in normal than in neoplastic tissues, and surface HLA-E was undetectable in most tumor cell lines. Herein, these issues were reinvestigated taking advantage of HLA-E-specific antibodies, immunohistochemistry, and biochemical methods detecting intracellular and surface HLA-E regardless of conformation. Contrary to published evidence, HLA-E was detected in a few normal epithelia and in a large fraction (approximately 1/3) of solid tumors, including those derived from HLA-E-negative/low-normal counterparts. Remarkably, HLA-E was detected in 30 of 30 tumor cell lines representative of major lymphoid and nonlymphoid lineages, and in 11 of 11, it was surface-expressed, although in a conformation poorly reactive with commonly used antibodies. Coexpression of HLA-E and HLA class I ligand donors was not required for surface expression but was associated with NKG2A-mediated protection from lysis by the cytotoxic cell line NKL and polyclonal NK cells from healthy donors, as demonstrated by antibody-mediated relief of protection in 10% to 20% of the tested target-effector combinations. NKG2A-mediated protection of additional targets became evident on NK effector blocking with antibodies to activating receptors (DNAM-1, natural cytotoxicity receptors, and NKG2D). Thus, initial evidence that the long-elusive HLA-E molecule is enhanced by malignant transformation and is functional in tumor cells is presented here, although its importance and precise functional role remain to be addressed in the context of a general understanding of the NK ligand-receptor network.

Indexed as

Cytotoxicity, ImmunologicAntibodies, MonoclonalAntigens, Differentiation, T-LymphocyteCell LineCell Line, TumorCell Transformation, NeoplasticHistocompatibility Antigens Class IHLA-E AntigensHumansKiller Cells, NaturalLymphocyte ActivationNeoplasmsNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily KReceptors, Natural Killer CellT Lineage-Specific Activation Antigen 1Antibodies, MonoclonalAntigens, Differentiation, T-LymphocyteHistocompatibility Antigens Class IHLA-E AntigensKLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily KReceptors, Natural Killer CellT Lineage-Specific Activation Antigen 1

Identifiers

PMID21969815
PMCPMC3182274
OpenAlexW1901034394

What OpenQuestion holds

Textmetadata
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.