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A “Toll Bridge” for Tumor-Specific T Cells

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Abstract

Toll-like receptors are among the fundamental molecules that alert the immune system to the presence of an infection by recognizing pathogen-associated molecules. The engagement of TLRs results in the activation of the adaptive immune system and the production of inflammatory molecules and various chemokines. Much of our understanding regarding TLR function stems from the study of innate immune cells, such as dendritic cells and macrophages. However, emerging studies from various groups, including ours, have shown that TLRs are expressed on CD4+ and CD8+ T cells and can function as costimulatory molecules. The engagement of TLRs on various T cell subsets enhances cell survival, proliferation, and/or increases the production of cytokines and effector molecules. These findings reveal a novel role for TLR agonists and may inspire new approaches in the development of immunotherapies and vaccines that are more effective by targeting or manipulating TLR signaling within T cells.

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Acknowledgments

This work was supported by a National Institutes of Health (NIH) Center for Biomedical Research Excellence Grant (1P20RR021970) and the Louisiana Cancer Research Consortium NIH grant number 1R01CA140917–0109 as a source of support.

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Correspondence to Eduardo Davila .

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Davila, E. (2009). A “Toll Bridge” for Tumor-Specific T Cells. In: Lustgarten, J., Cui, Y., Li, S. (eds) Targeted Cancer Immune Therapy. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-0170-5_10

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