Russian scientists have created a genetic model to help understand how the body suppresses autoimmune and neoplastic diseases. The scientists studied the properties of the Foxp3 protein which is responsible for Treg cell development and normal function. They found that removal of the Foxp3 protein gene from genomic DNA blocks Treg cell development and leads to biological death.
Many autoimmune diseases are associated with Foxp3 synthesis and abnormal numbers of Treg cells. The Foxp3 protein does not act alone, but as part of a protein complex that serves the genes essential for normal functioning of Treg cells. This group of proteins also includes Foxp1.
The researchers established a genetic model to explain how Foxp1 affects Foxp3. They first removed part of the Foxp1 gene from Treg from experimental mice. Comparing "normal" cells with Foxp1-depleted cells, it was found that Foxp3 has a much poorer ability to bind DNA without Foxp1. That means protein-coding genes that are critical for the normal function of Treg cells do not work properly without Foxp1. Therefore, Foxp3 is required for Treg, and Foxp1 is also very important, there is a negative impact on Foxp3 if the Foxp1 is removed. Understanding the structure of protein complexes composed of Foxp1 and Foxp3 is the key to making drugs that selectively affect Treg cells.
"The results broaden our understanding of the molecular mechanisms that regulate immune tolerance, which can be used to treat cancer and autoimmune diseases," the researchers said. "Cancerous tumors attract Treg cells to protect themselves from the body's immune system. The more Treg cells in a tumor, the worse the patient's prognosis. Therefore, if we can control the number and activity of Treg cells, we can reduce them in the tumor and increase them in the case of autoimmune diseases. It is possible to create safe drugs to treat diseases that have not been cured so far."
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