Abstract
Abstract The dysfunction of natural killer (NK) cells and T cells in acute myeloid leukemia (AML) determines the course of disease, but only limited information is available on the mechanisms of lymphocyte inhibition. This study aimed to evaluate to what extent malignant AML cells utilize NADPH-oxidase derived reactive oxygen species (ROS) as an immune evasion strategy. We report that a subset of genetically defined malignant monocytic AML cells (FAB class M4/M5), recovered from blood or bone marrow of untreated AML patients at diagnosis, express gp91phox, a component of the NADPH oxidase. These AML cells produced large amounts of ROS upon activation and triggered PARP 1-dependent apoptosis in adjacent natural killer (NK) cells, CD4+ T cells, and cytotoxic T cells. In contrast, myeloblastic (FAB class M2) or immature (FAB class M1) AML cells did not express gp91phox, did not produce ROS, and did not trigger NK or T cell apoptosis. Our data are suggestive of a novel mechanism by which monocytic AML cells evade lymphocyte immunity. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5414. doi:1538-7445.AM2012-5414
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
