Mary Brunkow | |
---|---|
Born | 1961 (age 63–64) Portland, Oregon, U.S. |
Education | University of Washington (BS) Princeton University (PhD) |
Known for | FOXP3 |
Awards | Nobel Prize in Physiology or Medicine (2025) |
Scientific career | |
Fields | Immunology Molecular biology |
Institutions | Institute for Systems Biology Celltech R&D |
Thesis | Expression and function of the H19 gene in transgenic mice (1991) |
Doctoral advisor | Shirley M. Tilghman |
Mary Elizabeth Brunkow [1] (born 1961) is an American molecular biologist and immunologist. 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.
Brunkow was born in 1961 in Portland, Oregon. [2] [3] She graduated at St. Mary's Academy in Portland in 1979. [3]
Brunkow received a Bachelor of Science with a major in molecular and cellular biology from the University of Washington in 1983 [4] and a Doctor of Philosophy in molecular biology from Princeton University in 1991. [5] Her advisor was Shirley M. Tilghman. [5] Her doctoral dissertation was titled Expression and function of the H19 gene in transgenic mice (1991). [1]
Brunkow worked in industry research in the Seattle area, at Celltech R&D in Bothell, Washington, which is where she and Fred Ramsdell performed their Nobel Prize-winning work on FOXP3, [6] and later she became senior program manager at the Institute for Systems Biology in Seattle. [7]
Brunkow is a co-author of the 2001 Nature Genetics paper that identified the scurfy gene product, initially termed scurfin and later known as FOXP3, linking its disruption to a fatal lymphoproliferative disorder in mice. [8] [9]
Brunkow's most cited work mapped the scurfy defect to FOXP3 and demonstrated that loss of this transcription factor drives uncontrolled T cell activation and lethal lymphoproliferation, positioning FOXP3 at the center of peripheral immune tolerance mediated by regulatory T cells. [8] [10] The genetic identification of FOXP3 provided a molecular basis for understanding how the immune system restrains self-reactivity outside the thymus and catalyzed extensive work on regulatory T cell development and function. [11] [12] Subsequent translational work by many groups led to anti-sclerostin therapy including romosozumab, which received regulatory approval and has been reviewed widely in the clinical literature. [13] [14]
On October 6, 2025, the Nobel Assembly at the Karolinska Institute in Stockholm, Sweden, announced that Brunkow, Fred Ramsdell, and Shimon Sakaguchi would share the Nobel Prize in Physiology or Medicine for discoveries concerning peripheral immune tolerance. [15] [16]