Immune Cell Function and Interaction
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This study demonstrates that selective depletion of arginase I (Arg1)-expressing tumor-associated macrophages (Arg1+ TAMs) inhibits tumor growth and concurrently reduces the ratio of TH1-Treg cells in the TME.
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The tumor microenvironment (TME) contains a number of immune-suppressive cells such as T helper 1-polarized regulatory T cells (TH1-Treg cells). However, little is known about the mechanism behind the abundant presence of TH1-Treg cells in the TME. We demonstrate that selective depletion of arginase I (Arg1)-expressing tumor-associated macrophages (Arg1+ TAMs) inhibits tumor growth and concurrently reduces the ratio of TH1-Treg cells in the TME. Arg1+ TAMs secrete the chemokine platelet factor 4 (PF4), which reinforces interferon-γ (IFN-γ)-induced Treg cell polarization into TH1-Treg cells in a manner dependent on CXCR3 and the IFN-γ receptor. Both genetic PF4 inactivation and PF4 neutralization hinder TH1-Treg cell accumulation in the TME and reduce tumor growth. Collectively, our study highlights the importance of Arg1+ TAM-produced PF4 for high TH1-Treg cell levels in the TME to suppress antitumor immunity.
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@article{Kuratani2024Platelet,
title = {Platelet factor 4–induced T H 1-T reg polarization suppresses antitumor immunity},
author = {Ayumi Kuratani and Masaaki Okamoto and Kazuki Kishida and Daisuke Okuzaki and Miwa Sasai and Shimon Sakaguchi and Hisashi Arase and Masahiro Yamamoto},
journal = {Science},
year = {2024},
doi = {10.1126/science.adn8608},
url = {https://doi.org/10.1126/science.adn8608}
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