DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Heung Kyu | ko |
dc.date.accessioned | 2021-09-13T00:30:25Z | - |
dc.date.available | 2021-09-13T00:30:25Z | - |
dc.date.created | 2021-09-12 | - |
dc.date.issued | 2021-06-04 | - |
dc.identifier.citation | KAI International Meeting 2021 Hybrid, pp.176 | - |
dc.identifier.uri | http://hdl.handle.net/10203/287726 | - |
dc.description.abstract | The anatomic location and immunologic characteristics of brain tumors result in strong lymphocyte suppression. Consequently, conventional immunotherapies targeting CD8 T cells are ineffective against brain tumors. Tumor cells escape immunosurveillance by various mechanisms, and tumor cell metabolism can affect the metabolic states and functions of tumor-infiltrating lymphocytes. Oxygen tension is one important factor influencing immune responses. Here, we discovered that brain tumor cells had a particularly high demand for oxygen, which affected γδ T cell-mediated antitumor immune responses but not those of conventional T cells. Specifically, tumor hypoxia activated the γδ T cell protein kinase A (PKA) pathway at a transcriptional level, resulting in repression of NKG2D expression. Alleviating tumor hypoxia reinvigorated NKG2D expression and the antitumor function of γδ T cells. These results reveal a hypoxia-mediated mechanism by which brain tumors and γδ T cells interact and emphasize the importance of γδ T cells for antitumor immunity against brain tumors. | - |
dc.language | English | - |
dc.publisher | The Korean Association of Immunologists | - |
dc.title | Tumor hypoxia represses γδ T cell-mediated antitumor immunity against brain tumors | - |
dc.type | Conference | - |
dc.type.rims | CONF | - |
dc.citation.beginningpage | 176 | - |
dc.citation.endingpage | 176 | - |
dc.citation.publicationname | KAI International Meeting 2021 Hybrid | - |
dc.identifier.conferencecountry | KO | - |
dc.identifier.conferencelocation | Virtual | - |
dc.contributor.localauthor | Lee, Heung Kyu | - |
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