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]
Research
Nobel Prize in Physiology or Medicine 2025: Pivotal role of FoxP3 Treg cells in peripheral immune tolerance.
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.[9][11] 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.[12][13]
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