Immune Cell Function and Interaction
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During acute infection, the transcriptional regulator inhibitor of DNA binding 3 (ID3) identifies stem-like T cells that are uniquely adapted to generate precursors of exhausted T (Tpex) cells in response to chronic infection or cancer.
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Stem-like T cells are attractive immunotherapeutic targets in patients with cancer given their ability to proliferate and differentiate into effector progeny. Thus, identifying T cells with enhanced stemness and understanding their developmental requirements are of broad clinical and therapeutic interest. Here, we demonstrate that during acute infection, the transcriptional regulator inhibitor of DNA binding 3 (ID3) identifies stem-like T cells that are uniquely adapted to generate precursors of exhausted T (Tpex) cells in response to chronic infection or cancer. Expression of ID3 itself enables Tpex cells to sustain T cell responses in chronic infection or cancer, whereas loss of ID3 results in impaired maintenance of CD8 T cell immunity. Furthermore, we demonstrate that interleukin-1 (IL-1) family members, including IL-36β and IL-18, promote the generation of ID3+ T cells that mediate superior tumor control. Overall, we identify ID3 as a common denominator of stem-like T cells in both acute and chronic infections that is specifically required to sustain T cell responses to chronic stimulation.
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@article{Graa2025Stem,
title = {Stem-like memory and precursors of exhausted T cells share a common progenitor defined by ID3 expression},
author = {Catarina Gago da Graça and Amania A. Sheikh and Dane M. Newman and Lifen Wen and S F. Li and Jian Shen and Yuqi Zhang and Sarah S. Gabriel and David Chisanga and Justine Jia Wen Seow and A Poch and L Rausch and Minh-Hanh Thi Nguyen and Jayendra Singh and Chun-Hsi Su and Leonie A. Cluse and Carlson Tsui and Thomas N. Burn and Simone L. Park and Bianca von Scheidt and Laura K. Mackay and Ajithkumar Vasanthakumar and David Bending and Wei Shi and Weiguo Cui and Jan Schröder and Ricky W. Johnstone and Axel Kallies and Daniel T. Utzschneider},
journal = {Science Immunology},
year = {2025},
doi = {10.1126/sciimmunol.adn1945},
url = {https://doi.org/10.1126/sciimmunol.adn1945}
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