The complement system as a regulator of tumor-promoting activities mediated by myeloid-derived suppressor cells
Tumor progression relies on the interaction between tumor cells and their surrounding tumor microenvironment (TME), which also influences therapeutic responses. The complement system, an essential part of innate im- munity, has been traditionally considered an effector arm against tumors. However, e...
| Autores: | , , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2022 |
| País: | España |
| Institución: | Universidad de Navarra |
| Repositorio: | Dadun. Depósito Académico Digital de la Universidad de Navarra |
| Idioma: | inglés |
| OAI Identifier: | oai:dadun.unav.edu:10171/65842 |
| Acceso en línea: | https://hdl.handle.net/10171/65842 |
| Access Level: | acceso abierto |
| Palabra clave: | Cancer immunity Complement system Myeloid-derived suppressor cells Complement-derived fragments Tumor microenvironment Immunotherapy C5a C5aR1 |
| Sumario: | Tumor progression relies on the interaction between tumor cells and their surrounding tumor microenvironment (TME), which also influences therapeutic responses. The complement system, an essential part of innate im- munity, has been traditionally considered an effector arm against tumors. However, established tumors co-opt complement-mediated immune responses in the TME to support chronic inflammation, activate cancer-related signaling pathways and hamper antitumor immune responses. In this context, myeloid-derived suppressor cells (MDSCs), a heterogeneous population of myeloid progenitors with immunosuppressive functions, are recognized as major mediators of tumor-associated complement activities. This review focuses on the impact of complement activation within the TME, with a special emphasis on MDSC functions and the involvement of the C5a/C5aR1 axis. We also discuss the translation of these findings into therapeutic advances based on comple- ment inhibition. |
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