| Literature DB >> 33087928 |
Ming Liu1, Fengshen Kuo2, Kristelle J Capistrano1, Davina Kang1, Briana G Nixon1,3, Wei Shi1, Chun Chou1, Mytrang H Do1,3, Efstathios G Stamatiades1, Shengyu Gao1,4, Shun Li1, Yingbei Chen5, James J Hsieh6, A Ari Hakimi2,7, Ichiro Taniuchi8, Timothy A Chan2, Ming O Li9,10,11.
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.Entities:
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Year: 2020 PMID： 33087928 PMCID： PMC8347705 DOI： 10.1038/s41586-020-2836-1
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 69.504