<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wurzer H</submitter><funding>Fonds National de la Recherche Luxembourg</funding><funding>Fonds De La Recherche Scientifique - FNRS</funding><funding>Fondation Cancer</funding><pagination>619069</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8181408</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12</volume><pubmed_abstract>Natural killer (NK) cells are innate effector lymphocytes with strong antitumor effects against hematologic malignancies such as chronic lymphocytic leukemia (CLL). However, NK cells fail to control CLL progression on the long term. For effective lysis of their targets, NK cells use a specific cell-cell interface, known as the immunological synapse (IS), whose assembly and effector function critically rely on dynamic cytoskeletal changes in NK cells. Here we explored the role of CLL cell actin cytoskeleton during NK cell attack. We found that CLL cells can undergo fast actin cytoskeleton remodeling which is characterized by a NK cell contact-induced accumulation of actin filaments at the IS. Such polarization of the actin cytoskeleton was strongly associated with resistance against NK cell</pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>Intrinsic Resistance of Chronic Lymphocytic Leukemia Cells to NK Cell-Mediated Lysis Can Be Overcome &lt;i>In Vitro&lt;/i> by Pharmacological Inhibition of Cdc42-Induced Actin Cytoskeleton Remodeling.</pubmed_title><pmcid>PMC8181408</pmcid><funding_grant_id>C19/BM/13579644, INTER/DFG/16/11509946</funding_grant_id><funding_grant_id>ACTIMMUNE, FC/2019/02</funding_grant_id><funding_grant_id>7.4536.19, 7.4531.20, 7.4503.19</funding_grant_id><pubmed_authors>Moussay E</pubmed_authors><pubmed_authors>Thomas C</pubmed_authors><pubmed_authors>Biolato AM</pubmed_authors><pubmed_authors>Hoffmann C</pubmed_authors><pubmed_authors>Mastio J</pubmed_authors><pubmed_authors>Largeot A</pubmed_authors><pubmed_authors>Krecke M</pubmed_authors><pubmed_authors>Paggetti J</pubmed_authors><pubmed_authors>Filali L</pubmed_authors><pubmed_authors>Francois JH</pubmed_authors><pubmed_authors>Wurzer H</pubmed_authors><pubmed_authors>Berchem G</pubmed_authors><pubmed_authors>De Wilde S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Intrinsic Resistance of Chronic Lymphocytic Leukemia Cells to NK Cell-Mediated Lysis Can Be Overcome &lt;i>In Vitro&lt;/i> by Pharmacological Inhibition of Cdc42-Induced Actin Cytoskeleton Remodeling.</name><description>Natural killer (NK) cells are innate effector lymphocytes with strong antitumor effects against hematologic malignancies such as chronic lymphocytic leukemia (CLL). However, NK cells fail to control CLL progression on the long term. For effective lysis of their targets, NK cells use a specific cell-cell interface, known as the immunological synapse (IS), whose assembly and effector function critically rely on dynamic cytoskeletal changes in NK cells. Here we explored the role of CLL cell actin cytoskeleton during NK cell attack. We found that CLL cells can undergo fast actin cytoskeleton remodeling which is characterized by a NK cell contact-induced accumulation of actin filaments at the IS. Such polarization of the actin cytoskeleton was strongly associated with resistance against NK cell</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2026-05-01T03:06:39.955Z</modification><creation>2022-02-10T14:36:12.402Z</creation></dates><accession>S-EPMC8181408</accession><cross_references><pubmed>34108958</pubmed><doi>10.3389/fimmu.2021.619069</doi></cross_references></HashMap>