FOXP3 in the context of Winged-helix transcription factors

⭐ Core Definition: FOXP3

FOXP3 (forkhead box P3), also known as scurfin, is a protein involved in immune system responses. A member of the FOX protein family, FOXP3 appears to function as a master regulator of the regulatory pathway in the development and function of regulatory T cells. Regulatory T cells generally turn the immune response down. In cancer, an excess of regulatory T cell activity can prevent the immune system from destroying cancer cells. In autoimmune disease, a deficiency of regulatory T cell activity can allow other autoimmune cells to attack the body's own tissues.

While the precise control mechanism has not yet been established, FOX proteins belong to the forkhead/winged-helix family of transcriptional regulators and are presumed to exert control via similar DNA binding interactions during transcription. In regulatory T cell model systems, the FOXP3 transcription factor occupies the promoters for genes involved in regulatory T-cell function, and may inhibit transcription of key genes following stimulation of T cell receptors.

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⭐ Core Definition: FOXP3
FOXP3 in the context of Regulatory T cell
FOXP3 in the context of Mary E. Brunkow

FOXP3 in the context of Regulatory T cell

The regulatory T cells (Tregs /ˈtiːrɛɡ/ or T_reg cells), formerly known as suppressor T cells, are a subpopulation of T cells that modulate the immune system, maintain tolerance to self-antigens, and prevent autoimmune disease. T_reg cells are immunosuppressive and generally suppress or downregulate induction and proliferation of effector T cells. T_reg cells express the biomarkers CD4, FOXP3, and CD25 and are thought to be derived from the same lineage as naïve CD4 cells. Because effector T cells also express CD4 and CD25, T_reg cells are very difficult to effectively discern from effector CD4, making them difficult to study. Research has found that the cytokine transforming growth factor beta (TGF-β) is essential for T_reg cells to differentiate from naïve CD4 cells and is important in maintaining T_reg cell homeostasis.

Mouse models have suggested that modulation of T_reg cells can treat autoimmune disease and cancer and can facilitate organ transplantation and wound healing. Their implications for cancer are complicated. T_reg cells tend to be upregulated in individuals with cancer, and they seem to be recruited to the site of many tumors. Studies in both humans and animal models have implicated that high numbers of T_reg cells in the tumor microenvironment is indicative of a poor prognosis, and T_reg cells are thought to suppress tumor immunity, thus hindering the body's innate ability to control the growth of cancerous cells. Immunotherapy research is studying how regulation of T cells could possibly be utilized in the treatment of cancer.

View the full Wikipedia page for Regulatory T cell

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FOXP3 in the context of Mary E. Brunkow

Mary Elizabeth Brunkow (born 1961) is an American molecular biologist, immunologist and Nobel Prize laureate. She is known for co-identifying the gene later named FOXP3 as the cause of the scurfy mouse phenotype, a finding that became foundational for modern regulatory T cell biology.

In 2025, she was jointly awarded the Nobel Prize in Physiology or Medicine with Fred Ramsdell and Shimon Sakaguchi for their work in peripheral immune tolerance.

View the full Wikipedia page for Mary E. Brunkow

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