<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Haroun-Izquierdo A</submitter><funding>NCI NIH HHS</funding><pagination>e005577</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9628692</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(11)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Natural killer (NK) cells hold great promise as a source for allogeneic cell therapy against hematological malignancies, including acute myeloid leukemia (AML). Current treatments are hampered by variability in NK cell subset responses, a limitation which could be circumvented by specific expansion of highly potent single killer immunoglobulin-like receptor (KIR)&lt;sup>+&lt;/sup>NKG2C&lt;sup>+&lt;/sup> adaptive NK cells to maximize missing-self reactivity.&lt;h4>Methods&lt;/h4>We developed a GMP-compliant protocol to expand adaptive NK cells from cryopreserved cells derived from select third-party superdonors, that is, donors harboring large adaptive NK cell subsets with desired KIR specificities at baseline. We studied the adaptive state of the cell product (ADAPT-NK) by flow cytometry </pubmed_abstract><journal>Journal for immunotherapy of cancer</journal><pubmed_title>Adaptive single-KIR&lt;sup>+&lt;/sup>NKG2C&lt;sup>+&lt;/sup> NK cells expanded from select superdonors show potent missing-self reactivity and efficiently control HLA-mismatched acute myeloid leukemia.</pubmed_title><pmcid>PMC9628692</pmcid><funding_grant_id>P01 CA111412</funding_grant_id><pubmed_authors>Miller JS</pubmed_authors><pubmed_authors>Blomberg P</pubmed_authors><pubmed_authors>Sohlberg E</pubmed_authors><pubmed_authors>Krokeide SZ</pubmed_authors><pubmed_authors>Berggren S</pubmed_authors><pubmed_authors>Valamehr B</pubmed_authors><pubmed_authors>Onfelt B</pubmed_authors><pubmed_authors>Kremer V</pubmed_authors><pubmed_authors>Ljunggren HG</pubmed_authors><pubmed_authors>Hammer Q</pubmed_authors><pubmed_authors>Bendzick L</pubmed_authors><pubmed_authors>Bjorklund A</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Wikstrom K</pubmed_authors><pubmed_authors>Felices M</pubmed_authors><pubmed_authors>Momayyezi P</pubmed_authors><pubmed_authors>van Ooijen H</pubmed_authors><pubmed_authors>Kanaya M</pubmed_authors><pubmed_authors>Tjonnfjord G</pubmed_authors><pubmed_authors>Kveberg L</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Vincenti M</pubmed_authors><pubmed_authors>Cichocki F</pubmed_authors><pubmed_authors>Wiiger MT</pubmed_authors><pubmed_authors>Haroun-Izquierdo A</pubmed_authors><pubmed_authors>Netskar H</pubmed_authors><pubmed_authors>Hoglund P</pubmed_authors><pubmed_authors>Malmberg KJ</pubmed_authors><pubmed_authors>Hoel HJ</pubmed_authors><pubmed_authors>Alici E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Adaptive single-KIR&lt;sup>+&lt;/sup>NKG2C&lt;sup>+&lt;/sup> NK cells expanded from select superdonors show potent missing-self reactivity and efficiently control HLA-mismatched acute myeloid leukemia.</name><description>&lt;h4>Background&lt;/h4>Natural killer (NK) cells hold great promise as a source for allogeneic cell therapy against hematological malignancies, including acute myeloid leukemia (AML). Current treatments are hampered by variability in NK cell subset responses, a limitation which could be circumvented by specific expansion of highly potent single killer immunoglobulin-like receptor (KIR)&lt;sup>+&lt;/sup>NKG2C&lt;sup>+&lt;/sup> adaptive NK cells to maximize missing-self reactivity.&lt;h4>Methods&lt;/h4>We developed a GMP-compliant protocol to expand adaptive NK cells from cryopreserved cells derived from select third-party superdonors, that is, donors harboring large adaptive NK cell subsets with desired KIR specificities at baseline. We studied the adaptive state of the cell product (ADAPT-NK) by flow cytometry </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2026-07-16T18:34:17.271Z</modification><creation>2026-07-11T03:08:39.349Z</creation></dates><accession>S-EPMC9628692</accession><cross_references><pubmed>36319065</pubmed><doi>10.1136/jitc-2022-005577</doi></cross_references></HashMap>