CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma
Abstract Natural killer (NK) cells are powerful immune effectors, modulating their anti-tumor function through a balance activating and inhibitor ligands on their cell surface. Though still emerging, cancer immunotherapies utilizing NK cells are proving promising as a modality for the treatment of a...
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| Format: | Article |
| Language: | English |
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BMC
2020-06-01
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| Series: | Journal of Hematology & Oncology |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s13045-020-00913-2 |
| _version_ | 1818459711097274368 |
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| author | Kyle B. Lupo Sandro Matosevic |
| author_facet | Kyle B. Lupo Sandro Matosevic |
| author_sort | Kyle B. Lupo |
| collection | DOAJ |
| description | Abstract Natural killer (NK) cells are powerful immune effectors, modulating their anti-tumor function through a balance activating and inhibitor ligands on their cell surface. Though still emerging, cancer immunotherapies utilizing NK cells are proving promising as a modality for the treatment of a number of solid tumors, including glioblastoma (GBM) and other gliomas, but are often limited due to complex immunosuppression associated with the GBM tumor microenvironment which includes overexpression of inhibitory receptors on GBM cells. CD155, or poliovirus receptor (PVR), has recently emerged as a pro-tumorigenic antigen, overexpressed on GBM and contributing to increased GBM migration and aggressiveness. CD155 has also been established as an immunomodulatory receptor, able to both activate NK cells through interactions with CD226 (DNAM-1) and CD96 and inhibit them through interaction with TIGIT. However, NK cell TIGIT expression has been shown to be upregulated in cancer, establishing CD155 as a predominantly inhibitory receptor within the context of GBM and other solid tumors, and rendering it of interest as a potential target for antigen-specific NK cell-based immunotherapy. This review will explore the function of CD155 within GBM as it relates to tumor migration and NK cell immunoregulation, as well as pre-clinical and clinical targeting of CD155/TIGIT and the potential that this pathway holds for the development of emerging NK cell-based immunotherapies. |
| first_indexed | 2024-12-14T23:18:41Z |
| format | Article |
| id | doaj.art-b633a8e291024570882c0cf394c7fcd3 |
| institution | Directory Open Access Journal |
| issn | 1756-8722 |
| language | English |
| last_indexed | 2024-12-14T23:18:41Z |
| publishDate | 2020-06-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Hematology & Oncology |
| spelling | doaj.art-b633a8e291024570882c0cf394c7fcd32022-12-21T22:44:01ZengBMCJournal of Hematology & Oncology1756-87222020-06-0113111010.1186/s13045-020-00913-2CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastomaKyle B. Lupo0Sandro Matosevic1Department of Industrial and Physical Pharmacy, Purdue UniversityDepartment of Industrial and Physical Pharmacy, Purdue UniversityAbstract Natural killer (NK) cells are powerful immune effectors, modulating their anti-tumor function through a balance activating and inhibitor ligands on their cell surface. Though still emerging, cancer immunotherapies utilizing NK cells are proving promising as a modality for the treatment of a number of solid tumors, including glioblastoma (GBM) and other gliomas, but are often limited due to complex immunosuppression associated with the GBM tumor microenvironment which includes overexpression of inhibitory receptors on GBM cells. CD155, or poliovirus receptor (PVR), has recently emerged as a pro-tumorigenic antigen, overexpressed on GBM and contributing to increased GBM migration and aggressiveness. CD155 has also been established as an immunomodulatory receptor, able to both activate NK cells through interactions with CD226 (DNAM-1) and CD96 and inhibit them through interaction with TIGIT. However, NK cell TIGIT expression has been shown to be upregulated in cancer, establishing CD155 as a predominantly inhibitory receptor within the context of GBM and other solid tumors, and rendering it of interest as a potential target for antigen-specific NK cell-based immunotherapy. This review will explore the function of CD155 within GBM as it relates to tumor migration and NK cell immunoregulation, as well as pre-clinical and clinical targeting of CD155/TIGIT and the potential that this pathway holds for the development of emerging NK cell-based immunotherapies.http://link.springer.com/article/10.1186/s13045-020-00913-2Natural killer cellsGlioblastomaCD155TIGITImmunotherapy |
| spellingShingle | Kyle B. Lupo Sandro Matosevic CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma Journal of Hematology & Oncology Natural killer cells Glioblastoma CD155 TIGIT Immunotherapy |
| title | CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma |
| title_full | CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma |
| title_fullStr | CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma |
| title_full_unstemmed | CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma |
| title_short | CD155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma |
| title_sort | cd155 immunoregulation as a target for natural killer cell immunotherapy in glioblastoma |
| topic | Natural killer cells Glioblastoma CD155 TIGIT Immunotherapy |
| url | http://link.springer.com/article/10.1186/s13045-020-00913-2 |
| work_keys_str_mv | AT kyleblupo cd155immunoregulationasatargetfornaturalkillercellimmunotherapyinglioblastoma AT sandromatosevic cd155immunoregulationasatargetfornaturalkillercellimmunotherapyinglioblastoma |