Opening The Floodgates: SRC-3’s Role In Regulatory T Cell Suppression

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I am a scientist, businessman, author, and philanthropist. For nearly two decades, I was a professor at Harvard Medical School and Harvard School of Public Health where I founded two academic research departments, the Division of Biochemical Pharmacology and the Division of Human Retrovirology.

immune system into suppressing their enemies; inhibiting this suppression could open the floodgates and allow immune cells to target cancer.Opening the floodgates of the immune system could help the body fight cancer. As described in a previous installment, researchers at the Baylor College of Medicine successfully eliminated breast and prostate tumors in mice by altering the expression of a specific protein in their regulatory T cells.

What if we could release the floodgates? Reversing Treg suppression could free the deluge of immune cells to the tumor and restore the immune system’s anticancer activity. Examining the link between regulatory T cell suppression and cancer could lead to a viable therapeutic for solid tumors—one which other immunotherapies, such as CAR T therapy, struggle to address.

A list of 297 transcriptional coregulator proteins from the Nuclear Receptor Signaling Atlas was also assembled to determine what cells express SRC-3 the most. The team found that SRC-3 is the second-most correlated coregulator protein for Treg cells. To confirm this finding, the blood of three human donors was analyzed for transcript levels of the protein. Compared to other immune cells , Tregs expressed much higher levels of SRC-3.

Altogether, these findings reveal the crucial role of SRC-3 in Treg suppression in mice and humans, and how affecting SRC-3 expression changes Treg-associated genes. SRC-3, in response, may be a possible target for future cancer immunotherapies.continues this investigation by analyzing the connection between SRC-3 in Tregs and the tumor microenvironment.

 

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