Mary Elizabeth 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 Americanmolecular biologist andimmunologist. She is known for co-identifying the gene later namedFOXP3 as the cause of thescurfy mouse phenotype, a finding that became foundational for modernregulatory T cell biology.
In 2025, she was jointly awarded theNobel Prize in Physiology or Medicine withFred Ramsdell andShimon Sakaguchi for their work inperipheral immune tolerance.
Brunkow was born in 1961 inPortland, Oregon.[2][3] She graduated fromSt. Mary's Academy in Portland in 1979.[3]
Brunkow received aBachelor of Science with a major in molecular and cellular biology from theUniversity of Washington in 1983[4] and aDoctor of Philosophy inmolecular biology fromPrinceton University in 1991.[5] Her doctoral advisor wasShirley M. Tilghman.[5] Her doctoral dissertation was titledExpression and function of the H19 gene in transgenic mice (1991).[1]
Brunkow worked in industry research in the Seattle area, atCelltech R&D in Bothell, Washington, which is where she andFred Ramsdell performed their Nobel Prize-winning work on FOXP3,[6] and later she became senior program manager at theInstitute for Systems Biology in Seattle.[7]
Brunkow is a co-author of the 2001Nature Genetics paper that identified the scurfy gene product, initially termed scurfin and later known as FOXP3, linking its disruption to a fatallymphoproliferative 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.[9][11] Subsequent translational work by many groups led to anti-sclerostin therapy includingromosozumab, which received regulatory approval and has been reviewed widely in the clinical literature.[12][13]
On October 6, 2025, theNobel Assembly at the Karolinska Institute inStockholm, Sweden, announced that Brunkow,Fred Ramsdell, andShimon Sakaguchi would share theNobel Prize in Physiology or Medicine for discoveries concerning peripheral immune tolerance.[14][15]
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