Endogenous Glucocorticoid Signaling Regulates CD8+ T Cell Differentiation and Development of Dysfunction in the Tumor Microenvironment
Name
nihms-1629126.pdf
Description
Accepted version
Size
3.63 MB
Format
Adobe PDF
Checksum (MD5)
89eb741259fc5d6498ba0430f829e7b4
Author(s)
Acharya, Nandini
Madi, Asaf
Zhang, Huiyuan
Klapholz, Max
Escobar, Giulia
Dulberg, Shai
Christian, Elena
Ferreira, Michelle
Dixon, Karen O
Fell, Geoffrey
Date Issued
2020
Journal
Immunity
Publisher
Elsevier BV
Version
Author's final manuscript
Abstract
© 2020 Elsevier Inc. Acharya et al. uncover a gradient of increasing glucocorticoid signaling from naïve to dysfunctional CD8+ tumor-infiltrating lymphocytes. This gradient regulates effector transition and development of dysfunction. Glucocorticoid is produced locally by tumor-associated monocyte-macrophage lineage cells, and presence of active glucocorticoid signaling associates with poor response to immune checkpoint blockade.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
Ludwig Center for Molecular Oncology (Massachusetts Institute of Technology)
Howard Hughes Medical Institute
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs License
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1016/J.IMMUNI.2020.08.005
