Professor Kate Schroder heads the Inflammasome Laboratory at the Institute for Molecular Bioscience (IMB), University of Queensland, as an NHMRC RD Wright Fellow. Kate is also the Director of the IMB Centre for Inflammation and Disease Research, the former Chair of the IMB Diversity and Inclusion Committee (2018-2020), and an editorial board member for Science Signaling, Cell Death and Disease, and Clinical and Translational Immunology. Kate’s graduate studies with Prof David Hume defined novel macrophage activation mechanisms, and her PhD was awarded in 2005. Her subsequent postdoctoral research with Profs Hume and Sweet identified surprising inter-species divergence in the inflammatory programs of human versus mouse macrophages (PNAS USA, 2012). As an NHMRC CJ Martin Fellow in Switzerland, Kate then trained with Prof Jürg Tschopp, a pioneer in the fields of inflammasome and cell death signalling pathways. Kate returned to Australia, and was appointed an IMB Lab Head in 2013. Kate’s laboratory investigates the molecular mechanisms governing inflammasome activity and caspase activation, the cell biology of inflammation, cell death and host defence, and mechanisms of inflammasome inhibition by cellular pathways and new small molecule inhibitors. The Inflammasome Lab contributed to the development of small molecule inflammasome inhibitors that are currently in phase II clinical trials by the UQ start-up company, Inflazome Ltd, as novel anti-inflammatory therapeutics. Inflazome Ltd was recently acquired by Roche to progress these drug candidates to the clinic. Kate served on the Inflazome Scientific Advisory Board from 2016-2017, and serves as a consultant for biotech and big pharmaceutical companies.
Kate Schroder在研究生期间与 David Hume教授共同完成的研究定义了新型的巨噬细胞激活机制，其于2005年获得博士学位。博士后阶段，Kate与Hume教授和Sweet教授发现人类与小鼠巨噬细胞的炎症程序存在令人惊讶的物种间差异（PNAS美国，2012年）。Kate曾在瑞士担任研究员，师从JürgTschopp教授，现任昆士兰大学分子生物科学研究所（IMB）炎症小体实验室负责人，IMB炎症和疾病研究中心主任， IMB多样性与包容委员会前主席（2018-2020），科学信号，细胞死亡和疾病以及临床和转化免疫学编辑委员会成员，NHMRC RD成员。Kate的实验室研究控制炎症小体活性和半胱天冬酶活化的分子机制，炎症的细胞生物学，细胞死亡和宿主防御以及通过细胞途径和新途径抑制炎症小体的机制。
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