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https://doi.org/10.1111/imcb.12309
Title: | Macrophages protect mycoplasma-infected chronic myeloid leukemia cells from natural killer cell killing | Authors: | Choo, Qing Wei Winnie Koean, Ricky Abdi Gunawan Chang, Shu-Chun Chng, Wee Joo Chan, Ming Chun Wang, Wilson Er, Jun Zhi Ding, Jeak Ling |
Keywords: | Science & Technology Life Sciences & Biomedicine Cell Biology Immunology Chronic infection inflammation chronic myeloid leukemia macrophages maintenance of NK mCD16 natural killer cells tumor environment NK CELLS BONE-MARROW CD16 ACTIVATION IDENTIFICATION EXPRESSION INTERLEUKIN-8 CYTOTOXICITY DYSFUNCTION CARCINOMA |
Issue Date: | 13-Jan-2020 | Publisher: | WILEY | Citation: | Choo, Qing Wei Winnie, Koean, Ricky Abdi Gunawan, Chang, Shu-Chun, Chng, Wee Joo, Chan, Ming Chun, Wang, Wilson, Er, Jun Zhi, Ding, Jeak Ling (2020-01-13). Macrophages protect mycoplasma-infected chronic myeloid leukemia cells from natural killer cell killing. IMMUNOLOGY AND CELL BIOLOGY 98 (2) : 138-151. ScholarBank@NUS Repository. https://doi.org/10.1111/imcb.12309 | Abstract: | Macrophages (Mϕ) have been reported to downmodulate the cytotoxicity of natural killer (NK) cell against solid tumor cells. However, the collaborative role between NK cells and Mϕ remains underappreciated, especially in hematological cancers, such as chronic myeloid leukemia (CML). We observed a higher ratio of innate immune cells (Mϕ and NK) to adaptive immune cells (T and B cells) in CML bone marrow aspirates, prompting us to investigate the roles of NK and Mϕ in CML. Using coculture models simulating the tumor inflammatory environment, we observed that Mϕ protects CML from NK attack only when CML was itself mycoplasma-infected and under chronic infection–inflammation condition. We found that the Mϕ-protective effect on CML was associated with the maintenance of CD16 level on the NK cell membrane. Although the NK membrane CD16 (mCD16) was actively shed in Mϕ + NK + CML trioculture, the NK mCD16 level was maintained, and this was independent of the modulation of sheddase by tissue inhibitor of metalloproteinase 1 or inhibitory cytokine transforming growth factor beta. Instead, we found that this process of NK mCD16 maintenance was conferred by Mϕ in a contact-dependent manner. We propose a new perspective on anti-CML strategy through abrogating Mϕ-mediated retention of NK surface CD16. | Source Title: | IMMUNOLOGY AND CELL BIOLOGY | URI: | https://scholarbank.nus.edu.sg/handle/10635/193733 | ISSN: | 08189641 14401711 |
DOI: | 10.1111/imcb.12309 |
Appears in Collections: | Elements Staff Publications |
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Choo et al (ICB_2020), Ding Lab_doi 10.1111imcb.12309 (main+suppl).pdf | Published version | 4.09 MB | Adobe PDF | OPEN | Published | View/Download |
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