Evidence map›Paper›PMID 26961084›Full record

ArticleCancer immunology, immunotherapy : CII2016

Immune checkpoint inhibitors enhance cytotoxicity of cytokine-induced killer cells against human myeloid leukaemic blasts.

Su Li Poh, Yeh Ching Linn

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
5.4field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  16. The Methylation inImmunoTargets and therapy · 2023
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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.

Su Li PohDepartment of Haematology, Singapore General Hospital, Level 3, Academia, 20, College Road, Singapore, 169856, Singapore.
Yeh Ching LinnDepartment of Haematology, Singapore General Hospital, Level 3, Academia, 20, College Road, Singapore, 169856, Singapore. linn.yeh.ching@sgh.com.sg.ORCID http://orcid.org/0000-0001-8098-2590
Singapore General Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We studied whether blockade of inhibitory receptors on cytokine-induced killer (CIK) cells by immune checkpoint inhibitors could increase its anti-tumour potency against haematological malignancies. CIK cultures were generated from seven normal donors and nine patients with acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL) or multiple myeloma (MM). The inhibitory receptors B and T lymphocyte attenuator, CD200 receptor, lymphocyte activation gene-3 (LAG-3) and T cell immunoglobulin and mucin-domain-containing-3 (TIM-3) were present at variable percentages in most CIK cultures, while cytotoxic T lymphocyte-associated protein 4 (CTLA-4), programmed death-1 (PD-1) and killer cell immunoglobulin-like receptors (KIR2DL1/2/3) were expressed at low level in most cultures. Without blockade, myeloid leukaemia cells were susceptible to autologous and allogeneic CIK-mediated cytotoxicity. Blockade of KIR, LAG-3, PD-1 and TIM-3 but not CTLA-4 resulted in remarkable increase in killing against these targets, even in those with poor baseline cytotoxicity. ALL and MM targets were resistant to CIK-mediated cytotoxicity, and blockade of receptors did not increase cytotoxicity to a meaningful extent. Combination of inhibitors against two receptors did not further increase cytotoxicity. Interestingly, potentiation of CIK killing by blocking antibodies was not predicted by expression of receptors on CIK and their respective ligands on the targets. Compared to un-activated T and NK cells, blockade potentiated the cytotoxicity of CIK cells to a greater degree and at a lower E:T ratio, but without significant increase in cytotoxicity against normal white cell. Our findings provide the basis for clinical trial combining autologous CIK cells with checkpoint inhibitors for patients with AML.

Indexed as

Acute DiseaseAntibodies, MonoclonalAntigens, SurfaceCell Line, TumorCTLA-4 AntigenCytokine-Induced Killer CellsCytotoxicity, ImmunologicCytotoxicity Tests, ImmunologicHepatitis A Virus Cellular Receptor 2HumansLeukemia, MyeloidMembrane ProteinsNeoplastic Stem CellsOrexin ReceptorsProgrammed Cell Death 1 ReceptorReceptors, Cell SurfaceAntibodies, MonoclonalAntigens, SurfaceCD200R1 protein, humanCTLA-4 AntigenHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2Membrane ProteinsOrexin ReceptorsPDCD1 protein, humanProgrammed Cell Death 1 ReceptorReceptors, Cell SurfaceReceptors, KIRCytokine-induced killer cellsImmune checkpoint inhibitorsInhibitory receptor and ligandMyeloid leukaemia

Identifiers

PMID26961084
PMCPMC11029729
OpenAlexW2296403803

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.