Journal
ONCOTARGET
Volume 7, Issue 8, Pages 8771-8782Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.6822
Keywords
sialic acid; tumor; immune regulation; regulatory T cells; natural killer cells
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Funding
- program of Marie Curie actions (7th Framework Programme for Research and Technological Development-Carmusys)
- KWF [VU2009-2598]
- NanoNextInitiative [3D01]
- European Research Council (ERC) [339977]
- European Research Council (ERC) [339977] Funding Source: European Research Council (ERC)
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The increased presence of sialylated glycans on the tumor surface has been linked to poor prognosis, yet the effects on tumor-specific T cell immunity are hardly studied. We here show that hypersialylation of B16 melanoma substantially influences tumor growth by preventing the formation of effector T cells and facilitating the presence of high regulatory T cell (Treg) frequencies. Knock-down of the sialic acid transporter created sialic acid low tumors, that grew slower in-vivo than hypersialylated tumors, altered the Treg/Teffector balance, favoring immunological tumor control. The enhanced effector T cell response in developing sialic acid low tumors was preceded by and dependent on an increased influx and activity of Natural Killer (NK) cells. Thus, tumor hypersialylation orchestrates immune escape at the level of NK and Teff/Treg balance within the tumor microenvironment, herewith dampening tumor-specific T cell control. Reducing sialylation provides a therapeutic option to render tumors permissive to immune attack.
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