Immunosurveillance of cancer cell stress
Authors:Seila Lorenzo-Herrero1-3, Christian Sordo-Bahamonde1-3, Segundo González1-3 and Alejandro López-Soto1-3
1 Departamento de Biología Funcional, Inmunología, Universidad de Oviedo, Oviedo, Spain.
2 Instituto Universitario de Oncología del Principado de Asturias (IUOPA) Oviedo, Spain.
3 Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain.
Keywords:
cancer, cell stress, immune system, tumor immunity, immunosurveillance.
Abbreviatons:
ATM – ataxia-telangiectasia mutated,
CML – chronic myelogenous leukemia,
CRT – calreticulin,
DC – dendritic cell,
DDR – DNA damage response,
ER – endoplasmic reticulum,
GZMB – granzyme B,
HIF – hypoxia-inducible factor,
HRE – hypoxia response element,
HSF – heat shock transcription factor,
HSP – heat shock protein,
ICB - immune checkpoint blockade,
IFNγ – interferon γ, LLC – Lewis lung carcinoma,
MDSC – myeloid-derived suppressor cell,
MHC – major histocompatibility complex,
MICA – MHC class I polypeptide-related sequence,
MM – multiple myeloma,
mTOR – mammalian target of rapamycin,
NK – natural killer,
ROS – reactive oxygen species,
TAM – tumor-associated macrophage,
TME – tumor microenvironment,
Treg – regulatory T cell,
UPR – unfolded protein response,
VEGF – vascular endothelial growth factor.
Corresponding Author(s):
Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Seila Lorenzo-Herrero, Christian Sordo-Bahamonde, Segundo González and Alejandro López-Soto (2019). Immunosur-veillance of cancer cell stress. Cell Stress 3(9): 295-309. doi: 10.15698/cst2019.09.198
© 2019 Lorenzo-Herrero et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and re-production in any medium, provided the original author and source are acknowledged.
Abstract:
Cancer development is tightly controlled by effector immune responses that recognize and eliminate malignantly transformed cells. Nonetheless, certain immune subsets, such as tumor-associated macrophages, have been described to promote tumor growth, unraveling a double-edge role of the immune system in cancer. Cell stress can modulate the crosstalk between immune cells and tumor cells, reshaping tumor immunogenicity and/or immune function and phenotype. Infiltrating immune cells are exposed to the challenging conditions typically present in the tumor microenvironment. In return, the myriad of signaling pathways activated in response to stress conditions may tip the balance toward stimulation of antitumor responses or immune-mediated tumor progression. Here, we explore how distinct situations of cellular stress influence innate and adaptive immunity and the consequent impact on cancer establishment and progression.