Blockade of TGF-β signaling to enhance the antitumor response is accompanied by dysregulation of the functional activity of CD4

Publication Title

Journal of translational medicine [electronic resource]

Authors

Magdalena J Polanczyk, Earle A. Chiles Research Institute, Providence Cancer Center, Portland, OR, USA
Edwin Walker, Earle A. Chiles Research Institute, Providence Cancer Center, Portland, OR, USA
Daniel Haley, Earle A. Chiles Research Institute, Providence Cancer Center, Portland, OR, USA
Bella S Guerrouahen
Emmanuel T Akporiaye, Earle A. Chiles Research Institute, Providence Cancer Center, Portland, OR, USAFollow

Document Type

Article

Publication Date

7-9-2019

Abstract

BACKGROUND: The pleiotropic cytokine, transforming growth factor (TGF)-β, and CD4

METHODS: Using BALB/c, FoxP3eGFP and Rag

RESULTS: SM16 abrogates TGF-β-induced Treg generation in vitro but does not prevent global homeostatic expansion of CD4

CONCLUSIONS: These findings suggest that blockade of TGF-β signaling is a potentially useful strategy for blunting Treg function to enhance the anti-tumor response. Our data further suggest that the overall dampening of Treg function may involve the expansion of a quiescent Treg precursor population, which is CD4

Area of Special Interest

Cancer

Specialty/Research Institute

Earle A. Chiles Research Institute

Specialty/Research Institute

Oncology