TGFβ suppresses CD8+ T cell expression of CXCR3 and tumor trafficking.
Publication Title
Nat Commun
Authors
Andrew J Gunderson, Earle A. Chiles Research Institute, Providence Portland Medical Center, Portland, OregonFollow
Tomoko Yamazaki, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, Portland, OR, 97213, USAFollow
Kayla McCarty, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Cancer Institute, Portland, OR, United States of AmericaFollow
Nathaniel E Fox, Earle A. Chiles Research Institute, Portland, OR 97213Follow
Michaela Phillips, Earle A. Chiles Research Institute, Providence Cancer Institute
Alejandro F Alice, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, PortlandFollow
Tiffany Blair, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, PortlandFollow
Mark Whiteford, Earle A. Chiles Research Institute, Providence Cancer InstituteFollow
David O'Brien, Earle A. Chiles Research Institute, Providence Cancer Institute
Rehan Ahmad, Earle A. Chiles Research Institute, Providence Cancer Institute
Maria X Kiely, Earle A. Chiles Research Institute, Providence Cancer InstituteFollow
Amanda Hayman, Earle A. Chiles Research Institute, Providence Cancer InstituteFollow
Todd Crocenzi, Earle A. Chiles Research Institute, Providence Cancer Institute
Michael J. Gough, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, PortlandFollow
Marka R. Crittenden, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, PortlandFollow
Kristina H YoungFollow
Publication Date
4-9-2020
Abstract
Transforming growth factor beta (TGFβ) is a multipotent immunosuppressive cytokine. TGFβ excludes immune cells from tumors, and TGFβ inhibition improves the efficacy of cytotoxic and immune therapies. Using preclinical colorectal cancer models in cell type-conditional TGFβ receptor I (ALK5) knockout mice, we interrogate this mechanism. Tumor growth delay and radiation response are unchanged in animals with Treg or macrophage-specific ALK5 deletion. However, CD8αCre-ALK5
Area of Special Interest
Cancer
Specialty/Research Institute
Oncology
Specialty/Research Institute
Earle A. Chiles Research Institute
