Literature DB >> 25542695

The bone marrow microenvironment is a critical player in the NK cell response against acute myeloid leukaemia in vitro.

Jochen Vasold1, Michaela Wagner1, Heidrun Drolle1, Christian Deniffel1, Alexander Kütt1, Robert Oostendorp2, Silvia Sironi1, Christina Rieger1, Michael Fiegl3.   

Abstract

Immune therapy for acute myeloid leukaemia (AML) has been largely disappointing. One possible explanation might lie in the microenvironment of the bone marrow, comprising cellular (e.g. mesenchymal stromal cells, MSC) and non-cellular components (e.g. hypoxia). The purpose of this study was to investigate the effects of these components in the immune response against AML in vitro. In vitro exposure of lymphocytes to hypoxia resulted in an increased expression of CD69 as an activation marker in NK cells only, with subsequently enhanced cell lysis of K-562 cell line by NK cells but not in lysis of primary blast. However, co-culture of AML cells with MSC significantly protected leukemic blasts from NK cell mediated lysis, mainly in a specific manner requiring cell-to-cell contact with supportive MSC. These data imply a relevant but unequivocal role of hypoxia and MSC the immune response against AML blasts.
Copyright © 2014 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Acute myeloid leukaemia; Hypoxia; Immune response; Mesenchymal stromal cells; NK cells

Mesh:

Year:  2014        PMID: 25542695     DOI: 10.1016/j.leukres.2014.12.001

Source DB:  PubMed          Journal:  Leuk Res        ISSN: 0145-2126            Impact factor:   3.156


  16 in total

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Journal:  Front Immunol       Date:  2019-10-11       Impact factor: 7.561

Review 9.  Optimizing NK Cell-Based Immunotherapy in Myeloid Leukemia: Abrogating an Immunosuppressive Microenvironment.

Authors:  Natasha Mupeta Kaweme; Fuling Zhou
Journal:  Front Immunol       Date:  2021-06-17       Impact factor: 7.561

10.  The bone marrow microenvironment enhances multiple myeloma progression by exosome-mediated activation of myeloid-derived suppressor cells.

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