TGF-β suppresses type 2 immunity to cancer

Ming Liu, Fengshen Kuo, Kristelle J. Capistrano, Davina Kang, Briana G. Nixon, Wei Shi, Chun Chou, Mytrang H. Do, Efstathios G. Stamatiades, Shengyu Gao, Shun Li, Yingbei Chen, James J. Hsieh, A. Ari Hakimi, Ichiro Taniuchi, Timothy A. Chan and Ming O. Li ()
Additional contact information
Ming Liu: Memorial Sloan Kettering Cancer Center
Fengshen Kuo: Memorial Sloan Kettering Cancer Center
Kristelle J. Capistrano: Memorial Sloan Kettering Cancer Center
Davina Kang: Memorial Sloan Kettering Cancer Center
Briana G. Nixon: Memorial Sloan Kettering Cancer Center
Wei Shi: Memorial Sloan Kettering Cancer Center
Chun Chou: Memorial Sloan Kettering Cancer Center
Mytrang H. Do: Memorial Sloan Kettering Cancer Center
Efstathios G. Stamatiades: Memorial Sloan Kettering Cancer Center
Shengyu Gao: Memorial Sloan Kettering Cancer Center
Shun Li: Memorial Sloan Kettering Cancer Center
Yingbei Chen: Memorial Sloan Kettering Cancer Center
James J. Hsieh: Washington University
A. Ari Hakimi: Memorial Sloan Kettering Cancer Center
Ichiro Taniuchi: RIKEN Center for Integrative Medical Sciences
Timothy A. Chan: Memorial Sloan Kettering Cancer Center
Ming O. Li: Memorial Sloan Kettering Cancer Center

Nature, 2020, vol. 587, issue 7832, 115-120

Abstract: Abstract The immune system uses two distinct defence strategies against infections: microbe-directed pathogen destruction characterized by type 1 immunity1, and host-directed pathogen containment exemplified by type 2 immunity in induction of tissue repair2. Similar to infectious diseases, cancer progresses with self-propagating cancer cells inflicting host-tissue damage. The immunological mechanisms of cancer cell destruction are well defined3–5, but whether immune-mediated cancer cell containment can be induced remains poorly understood. Here we show that depletion of transforming growth factor-β receptor 2 (TGFBR2) in CD4+ T cells, but not CD8+ T cells, halts cancer progression as a result of tissue healing and remodelling of the blood vasculature, causing cancer cell hypoxia and death in distant avascular regions. Notably, the host-directed protective response is dependent on the T helper 2 cytokine interleukin-4 (IL-4), but not the T helper 1 cytokine interferon-γ (IFN-γ). Thus, type 2 immunity can be mobilized as an effective tissue-level defence mechanism against cancer.

Date: 2020
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DOI: 10.1038/s41586-020-2836-1

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