<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>17</volume><submitter>Kelm M</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Blinatumomab (BLN) is a bispecific T-cell engager that has revolutionized the treatment of B-cell precursor acute lymphoblastic leukemia (BCP-ALL), significantly improving outcomes in both adults and children. By simultaneously binding to CD19 on B cells and CD3 on T cells, BLN triggers target cell-dependent T-cell activation, resulting in the cytolysis of CD19&lt;sup>+&lt;/sup> BCP-ALL cells. Despite the remarkable clinical advancements achieved with BLN, the immunological mechanisms underlying treatment response or failure remain poorly characterized. γδ T cells are attractive candidates for adoptive T-cell therapy due to potent cytotoxicity, capacity to present antigens, broad lysis of different tumor entities, and low alloreactivity. Because γδ T cells can also be redire</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1739493</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12920462</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Blinatumomab-driven T-cell activation in αβ and γδ T-cell subsets: insights from &amp;lt;i&amp;gt;in vitro&amp;lt;/i&amp;gt; assays.</pubmed_title><pmcid>PMC12920462</pmcid><pubmed_authors>Bendig S</pubmed_authors><pubmed_authors>Peters C</pubmed_authors><pubmed_authors>Kabelitz D</pubmed_authors><pubmed_authors>Nasr N</pubmed_authors><pubmed_authors>Laqua A</pubmed_authors><pubmed_authors>Janssen O</pubmed_authors><pubmed_authors>Trautmann H</pubmed_authors><pubmed_authors>Baldus CD</pubmed_authors><pubmed_authors>Chitadze G</pubmed_authors><pubmed_authors>Scheffold A</pubmed_authors><pubmed_authors>Wesch D</pubmed_authors><pubmed_authors>Kelm M</pubmed_authors><pubmed_authors>Lustig M</pubmed_authors><pubmed_authors>Oberg HH</pubmed_authors><pubmed_authors>Bruggemann M</pubmed_authors><pubmed_authors>Valerius T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Blinatumomab-driven T-cell activation in αβ and γδ T-cell subsets: insights from &amp;lt;i&amp;gt;in vitro&amp;lt;/i&amp;gt; assays.</name><description>&lt;h4>Introduction&lt;/h4>Blinatumomab (BLN) is a bispecific T-cell engager that has revolutionized the treatment of B-cell precursor acute lymphoblastic leukemia (BCP-ALL), significantly improving outcomes in both adults and children. By simultaneously binding to CD19 on B cells and CD3 on T cells, BLN triggers target cell-dependent T-cell activation, resulting in the cytolysis of CD19&lt;sup>+&lt;/sup> BCP-ALL cells. Despite the remarkable clinical advancements achieved with BLN, the immunological mechanisms underlying treatment response or failure remain poorly characterized. γδ T cells are attractive candidates for adoptive T-cell therapy due to potent cytotoxicity, capacity to present antigens, broad lysis of different tumor entities, and low alloreactivity. Because γδ T cells can also be redire</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026</publication><modification>2026-07-16T18:06:56.547Z</modification><creation>2026-07-09T11:10:43.196Z</creation></dates><accession>S-EPMC12920462</accession><cross_references><pubmed>41727470</pubmed><doi>10.3389/fimmu.2026.1739493</doi></cross_references></HashMap>