Evidence map›Paper›PMID 30277471›Full record

ArticleThe Journal of clinical investigation2018

CD84 regulates PD-1/PD-L1 expression and function in chronic lymphocytic leukemia.

Hadas Lewinsky, Avital F Barak, Victoria Huber, Matthias P Kramer, Lihi Radomir, Lital Sever, Irit Orr, Vita Mirkin, Nili Dezorella, Mika Shapiro and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 70 citations in OpenAlex.

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  8. SLAM family-mediated crosstalk between tumor and immune cells in the tumor microenvironment: a promising biomarker and a potential therapeutic target for immune checkpoint therapies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
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  16. SLAM Family Receptors in B Cell Chronic Lymphoproliferative Disorders.International journal of molecular sciences · 2024
    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

16 authors at 5 institutions in 2 countries.

Hadas LewinskyDepartment of Immunology and.
Avital F BarakDepartment of Immunology and.
Victoria HuberDepartment of Immunology and.
Matthias P KramerDepartment of Immunology and.
Lihi RadomirDepartment of Immunology and.
Lital SeverDepartment of Immunology and.
Irit OrrLife Sciences Core Facilities, Department of Biochemistry, Weizmann Institute of Science, Rehovot, Israel.
Vita MirkinHematology Institute, Kaplan Medical Center, Rehovot, Israel.
Nili DezorellaDepartment of Hematology, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
Mika ShapiroDepartment of Hematology, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
Yosef CohenSanz Medical Center, Laniado Medical Center, Netanya, Israel.
Lev ShvidelHematology Institute, Kaplan Medical Center, Rehovot, Israel.
Martina SeiffertMolecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Yair HerishanuHematology Institute, Kaplan Medical Center, Rehovot, Israel.
Shirly Becker-HermanDepartment of Immunology and.
Idit ShacharDepartment of Immunology and.
Kaplan Medical Center · ILTel Aviv Sourasky Medical Center · ILGerman Cancer Research Center · DELaniado Hospital · ILWeizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) is characterized by clonal proliferation and progressive accumulation of mature B lymphocytes in the peripheral blood, lymphoid tissues, and bone marrow. CLL is characterized by profound immune defects leading to severe infectious complications. T cells are numerically, phenotypically, and functionally highly abnormal in CLL, with only limited ability to exert antitumor immune responses. Exhaustion of T cells has also been suggested to play an important role in antitumor responses. CLL-mediated T cell exhaustion is achieved by the aberrant expression of several inhibitory molecules on CLL cells and their microenvironment, prominently the programmed cell death ligand 1/programmed cell death 1 (PD-L1/PD-1) receptors. Previously, we showed that CD84, a member of the SLAM family of receptors, bridges between CLL cells and their microenvironment. In the current study, we followed CD84 regulation of T cell function. We showed that cell-cell interaction mediated through human and mouse CD84 upregulates PD-L1 expression on CLL cells and in their microenvironment and PD-1 expression on T cells. This resulted in suppression of T cell responses and activity in vitro and in vivo. Thus, our results demonstrate a role for CD84 in the regulation of immune checkpoints by leukemia cells and identify CD84 blockade as a therapeutic strategy to reverse tumor-induced immune suppression.

Indexed as

AnimalsB7-H1 AntigenGene Expression Regulation, LeukemicHumansLeukemia, Lymphocytic, Chronic, B-CellMiceMice, KnockoutNeoplasm ProteinsProgrammed Cell Death 1 ReceptorSignaling Lymphocytic Activation Molecule FamilyB7-H1 AntigenCD274 protein, humanCd274 protein, mouseCD84 protein, humanCd84 protein, mouseNeoplasm ProteinsPDCD1 protein, humanPdcd1 protein, mouseProgrammed Cell Death 1 ReceptorSignaling Lymphocytic Activation Molecule FamilyCellular immune responseImmunologyLeukemiasOncology

Identifiers

PMID30277471
PMCPMC6264738
OpenAlexW2895343571

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.