<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Inoue Y</submitter><funding>Japanese Society of Hematology</funding><funding>Research Clusters program of Tokushima University</funding><funding>Bristol Myers Squibb Foundation</funding><funding>Japan Society for the Promotion of Science</funding><pagination>559-563</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11786308</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>116(2)</volume><pubmed_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 an</pubmed_abstract><journal>Cancer science</journal><pubmed_title>Elotuzumab-mediated ADCC with Th1-like Vγ9Vδ2 T cells to disrupt myeloma-osteoclast interaction.</pubmed_title><pmcid>PMC11786308</pmcid><funding_grant_id>21H03111</funding_grant_id><funding_grant_id>JP23H03101</funding_grant_id><funding_grant_id>JP17H05104</funding_grant_id><funding_grant_id>23195</funding_grant_id><funding_grant_id>2202003</funding_grant_id><funding_grant_id>22K19626</funding_grant_id><funding_grant_id>JP22K08455</funding_grant_id><funding_grant_id>JP19K22719</funding_grant_id><pubmed_authors>Hiasa M</pubmed_authors><pubmed_authors>Maeda Y</pubmed_authors><pubmed_authors>Kagawa K</pubmed_authors><pubmed_authors>Ozaki S</pubmed_authors><pubmed_authors>Oda A</pubmed_authors><pubmed_authors>Endo I</pubmed_authors><pubmed_authors>Harada T</pubmed_authors><pubmed_authors>Maruhashi T</pubmed_authors><pubmed_authors>Fujii S</pubmed_authors><pubmed_authors>Abe M</pubmed_authors><pubmed_authors>Hara T</pubmed_authors><pubmed_authors>Oura M</pubmed_authors><pubmed_authors>Sumitani R</pubmed_authors><pubmed_authors>Sogabe K</pubmed_authors><pubmed_authors>Teramachi J</pubmed_authors><pubmed_authors>Takahashi M</pubmed_authors><pubmed_authors>Miki H</pubmed_authors><pubmed_authors>Inoue Y</pubmed_authors><pubmed_authors>Nakamura S</pubmed_authors><pubmed_authors>Tenshin H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Elotuzumab-mediated ADCC with Th1-like Vγ9Vδ2 T cells to disrupt myeloma-osteoclast interaction.</name><description>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 an</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2025-04-03T23:41:52.081Z</modification><creation>2025-04-03T23:41:52.081Z</creation></dates><accession>S-EPMC11786308</accession><cross_references><pubmed>39557586</pubmed><doi>10.1111/cas.16401</doi></cross_references></HashMap>