Monday, 3 October 2016

“TLR-mediated degradation of cIAP1 triggers cell death and inflammasome activation in the absence of XIAP." Thursday 6 October

This week's  Hudson Seminar will be held Thursday 6 Oct, 12-1 pm, Lecture Theatre 1, Monash Medical Centre.

The speaker will be Dr Kate Lawlor, Senior Postdoctoral Fellow, Vince Laboratory, Inflammation Division, Walter and Eliza Hall Institute of Medical Research.

Light refreshments to follow presentation outside the Lecture Theatre.

Dr Kate completed her PhD at the Walter and Eliza Hall Institute of Medical Research in 2004, where she discovered a pathogenic role for G-CSF in rheumatoid arthritis (phase 1 clinical trials underway, CSL). After being awarded a CJ Martin training Fellowship she completed a postdoctoral position at the Cambridge Institute for Medical Research (2005-2008, Prof K. Smith) examining the effects of innate inhibitory receptors on autoimmune and infectious diseases. Upon her return to WEHI, Kate has focused her research on the role of cell death regulators in inflammation. Her work has defined the role of Inhibitor of Apoptosis Proteins (IAPs), particularly XIAP, in repressing ripoptosome-mediated cell death and inflammasome activation.

Recently, Kate and her research team has uncovered that Toll-like receptors (TLR) utilising the adaptor Myd88 induce the degradation of cIAP1, and its binding partner TRAF2. Conversely, a TRIF-type 1 IFN signal blocks cIAP1 degradation. Notably, in the absence of XIAP, TLR-induced cIAP1 degradation activates the NLRP3 inflammasome. These results may explain why in response to pathogen infection, XIAP mutant patients may develop severe autoinflammatory symptoms characterised by enhanced inflammasome activity.

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