Home » Link Found Between T Cell Exhaustion and Sympathetic Stress Response in Cancer Patients, Opens New Avenues for Treatment

Link Found Between T Cell Exhaustion and Sympathetic Stress Response in Cancer Patients, Opens New Avenues for Treatment

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Scientists Discover Link Between T Cell Exhaustion and Sympathetic Stress Response in Cancer Treatment

Date: September 30, 2023

Scientists from the Salk Institute and other research institutions have made a significant breakthrough in cancer treatment by uncovering a link between T cell exhaustion and the body’s sympathetic stress response. The findings, based on studying multiple cancer types in mouse and human tissue samples, could potentially lead to the development of more resilient cancer-fighting cells.

Killer T cells, specialized immune cells that actively seek out and destroy cancer cells, can become exhausted, limiting their ability to effectively combat tumors. By understanding the reasons behind T cell exhaustion, scientists hope to enhance the body’s immune response to cancer.

In a recent article published in the prestigious scientific journal Nature, researchers from the Salk Institute and other institutions outlined their discovery of the connection between T cell exhaustion and the sympathetic stress response, also known as the “fight or flight” response. The study revealed that beta-blockers, commonly used drugs to control blood pressure and heart rate, may inhibit the interaction between killer T cells and sympathetic stress response hormones. By inhibiting this interaction, more effective cancer-fighting T cells can be produced.

The scientists involved in the study established an innovative link between the sympathetic stress response and how the immune system interacts with cancer. They also demonstrated that combining beta blockers with current immunotherapies has the potential to improve the immune system’s response by enhancing the function of killer T cells.

Professor Susan Kaech, one of the researchers involved in the study, stated that while immunotherapy has revolutionized cancer treatment, there are still patients who do not respond well to this approach. Understanding how the nervous system can inhibit the function of immune cells that destroy cancer opens up new possibilities for restoring T cell function in tumors.

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The sympathetic nervous system, responsible for the body’s stress response, plays a key role in mediating the interaction between nerves and the immune response against infection or cancer. In their study, the researchers focused on the sympathetic nerves that produce norepinephrine, a stress hormone. They found that norepinephrine binds to killer T cells through a receptor called ADRB1. Exhausted T cells express more ADRB1 receptors, impairing their function in fighting cancer.

To test the prevention of T cell exhaustion, the researchers experimented with blocking norepinephrine’s interaction with ADRB1. They discovered that by removing ADRB1 or using beta-blockers to impair its function, more functional killer T cells were produced. These T cells were able to effectively destroy cancer cells. The study also revealed that exhausted T cells were unable to “listen” to nerves from a distance but were drawn towards nerve tissue, further inhibiting their function in fighting cancer.

The researchers believe that understanding the relationship between nerves and exhausted T cells could lead to the development of new cancer therapies. By targeting this process, it may be possible to prevent the exhaustion of T cells and enhance their ability to fight tumors.

The scientists hope to expand their understanding by studying tissue samples from a wider range of human cancer patients. They aim to collaborate with clinicians to implement beta-blockers in lung cancer patients as soon as possible, providing further evidence of their efficacy in cancer therapy.

In summary, the groundbreaking study has uncovered a new mechanism for restoring the body’s anti-tumor ability by blocking CD8+ T cells. This discovery has the potential to significantly improve cancer treatment and provide hope for patients who do not respond well to current immunotherapies.

Image Source: Nature (2023). DOI:10.1038/s41586-023-06568-6

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Disclaimer: This article is a summary of the original source from Bioon.com. All rights reserved.

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