Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Apr 21;10:103–122. doi: 10.2147/ITT.S255224

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 Yang et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

PMC Copyright notice

Current understanding of the role of TNF-TNFR2 signaling in the tumor microenvironment. In the tumor microenvironment (TME), tumor-associated macrophages, effector cells (CD4⁺ and CD8⁺ T effector (Teff) cells and natural killer (NK) cells), and tumor cells are the major source of TNF. In response to TNF stimulation, the number of CD4⁺Foxp3⁺TNFR2⁺ Treg cells are increased. These expanded Treg cells in TME are more stable in phenotype and more immunosuppressive. Moreover, TNF activates TNFR2⁺ myeloid-derived suppressor cells (MDSCs) and TNFR2⁺ mesenchymal stem cells (MSCs). Tregs, MDSCs, and MSCs likely operate collaboratively in the inhibition of the anti-tumor immune response and the promotion of tumor evasion. Further, TNFR2 signaling also promotes the survival, metastasis, and growth of the tumor.