New tricks for XIAP in cell death and inflammation

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XIAP deficiency, also known as X-linked proliferative disease type 2 (XLP-2), is a rare disorder with a broad spectrum of symptoms, including severe hyperinflammation (haemophagocytic lymphohistiocytosis, HLH) and inflammatory bowel disease. Research, including our own, has shown that inflammasome activation can occur after priming in the absence of XIAP, and that TNF loss can prevent this activation. However, the failure of TNF biologics in XIAP-deficient patients suggests that TNF primarily initiates pro-inflammatory cytokine production but is no longer required once stimulation has occurred. Our group has investigated the role of TNF receptor 2 (TNFR2) in XIAP deficiency and identified an increased interferon-stimulated gene (ISG) signature. To further understand how XIAP regulates inflammasome activation, cell death, and interferon signaling, we are using diGLY ubiquitome mass spectrometry to identify its key substrates.



From 17 Apr 2025 14:00
Until 17 Apr 2025 15:00
Location FSVM I building, seminar room

Speaker Lynn Wong
Affiliation Department of Molecular Life Sciences, University of Zurich
Host Jonathan Maelfait

Stream View stream
Stream ID 817 6806 6014
Stream Password 051352

About the speaker

Lynn originally hails from the land of maple syrup, Canada. She completed her Bachelors at the University of Guelph (BSc Biochemistry) and her doctorate at the University of Toronto (PhD Medical Biophysics). She then left for warmer weather in Melbourne, Australia and briefly worked with Steve Gerondakis studying myelopoiesis and NF-kB signaling. Most of her time in Australia was spent on understanding the inhibitors of apoptosis proteins and receptor interacting serine/threonine protein kinases under John Silke and David Vaux. She established her research group at the Institute of Experimental Immunology, Faculty of Medicine, which is now based in the Department of Molecular Life Sciences, Faculty of Science. Her team investigates how molecular mechanisms of cell death signaling influence surrounding tissues, spanning from organelles to whole organisms.


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