Evidence map›Paper›PMID 39557586›Full record

ArticleCancer science2025

Elotuzumab-mediated ADCC with Th1-like Vγ9Vδ2 T cells to disrupt myeloma-osteoclast interaction.

Yusuke Inoue, Hirofumi Tenshin, Jumpei Teramachi, Ryohei Sumitani, Asuka Oda, Yusaku Maeda, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi and 10 more

Abstract read
In one paragraph

Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. T Cells Dysfunction in Multiple Myeloma.ImmunoTargets and therapy · 2025
    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

20 authors.

Yusuke InoueDepartment of Medical Technology, Tokushima University Hospital, Tokushima, Japan.
Hirofumi TenshinDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Jumpei TeramachiDepartment of Oral Function and Anatomy, Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Ryohei SumitaniDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Asuka OdaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Yusaku MaedaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Masahiro OuraDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Kimiko SogabeDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Tomoko MaruhashiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Mamiko TakahashiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Shiro FujiiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Shingen NakamuraDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Hirokazu MikiDivision of Transfusion Medicine and Cell Therapy, Tokushima University Hospital, Tokushima, Japan.
Tomoyo HaraDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Itsuro EndoDepartment of Bioregulatory Sciences, Tokushima University Hospital, Tokushima, Japan.
Kumiko KagawaDepartment of Hematology, Tokushima Prefectural Central Hospital, Tokushima, Japan.
Shuji OzakiDepartment of Hematology, Tokushima Prefectural Central Hospital, Tokushima, Japan.
Masahiro HiasaDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Takeshi HaradaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.ORCID https://orcid.org/0000-0002-3997-7471
Masahiro AbeDepartment of Hematology, Kawashima Hospital, Tokushima, Japan.

Funding

Bristol Myers Squibb FoundationJapanese Society of Hematology 23195Japan Society for the Promotion of Science 21H03111Japan Society for the Promotion of Science 22K19626Japan Society for the Promotion of Science JP17H05104Japan Society for the Promotion of Science JP19K22719Japan Society for the Promotion of Science JP22K08455Japan Society for the Promotion of Science JP23H03101Research Clusters program of Tokushima University 2202003
6 · The paper itself

Abstract

Multiple myeloma (MM) cells and osteoclasts (OCs) activate with each other to cause drug resistance. Human Th1-like Vγ9Vδ2 (γδ) T cells, important effectors against tumors, can be expanded and activated ex vivo by the aminobisphosphonate zoledronic acid in combination with IL-2. We previously reported that the expanded γδ T cells effectively targeted and killed OCs as well as MM cells. Because the expanded γδ T cells expressed CD16 on their surface, we investigated the utilization of the expanded γδ T cells for antibody-dependent cellular cytotoxicity (ADCC). Although the expanded γδ T cells alone induced cell death in MM cell lines, the addition of the anti-SLAMF7 monoclonal antibody elotuzumab (ELO) further enhanced their cytotoxic activity only against SLAMF7-expressing MM cell lines and primary MM cells. Intriguingly, ELO was also able to enhance γδ T cell-induced cell death against OCs cultured alone, and against both MM cells and OCs in their coculture settings. SLAMF7 was found to be highly expressed in OCs differentiated in vitro from monocytes by receptor activator of nuclear factor-κ B ligand and M-CSF, although monocytes only marginally expressed SLAMF7. These results demonstrate that SLAMF7 is highly expressed in both MM cells and OCs, and that the ex vivo-expanded γδ T cells can exert ELO-mediated ADCC against SLAMF7-expressing MM cells and OCs besides their direct cytotoxic activity. Further study is warranted for the innovative utilization of γδ T cells.

Indexed as

Antibodies, Monoclonal, HumanizedAntibody-Dependent Cell CytotoxicityMultiple MyelomaOsteoclastsTh1 CellsCell Line, TumorCoculture TechniquesDiphosphonatesHumansInterleukin-2Intraepithelial LymphocytesReceptors, Antigen, T-Cell, gamma-deltaSignaling Lymphocytic Activation Molecule FamilyZoledronic AcidAntibodies, Monoclonal, HumanizedDiphosphonateselotuzumabInterleukin-2Receptors, Antigen, T-Cell, gamma-deltaSignaling Lymphocytic Activation Molecule FamilySLAMF7 protein, humanZoledronic AcidElotuzumabmultiple myelomaosteoclastSLAMF7Vγ9Vδ2 T cell

Identifiers

PMID39557586
PMCPMC11786308

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.