<b>Dr Kate Schroder</b><br>
Group Leader, Cell Biology and Molecular Medicine Division<br>
Deputy Director, Centre for Inflammation and Disease Research<p>
P: +61 7 3346 2058<br>
E: k.schroder@imb.uq.edu.au<p>
- innate immunity<br>
- inflammasome<br>
- inflammation<br>
- caspase<br>
- Salmonella<br>
- hereditary diseases<br>
- diabetes<br>
- arthritis<br>
- gout
Dr Kate Schroder
Group Leader, Cell Biology and Molecular Medicine Division
Deputy Director, Centre for Inflammation and Disease Research

P: +61 7 3346 2058
E: k.schroder@imb.uq.edu.au

- innate immunity
- inflammasome
- inflammation
- caspase
- Salmonella
- hereditary diseases
- diabetes
- arthritis
- gout

Visit the IMB Inflammasome Lab website for more information.

Inflammasomes: mediators of immune defence but culprits in inflammatory disease  

The innate immune system is the body’s first line of defence against microbial attack. The innate immune system recognises situations of cellular danger through receptors such as NOD-like receptors (NLRs), which sense microbial structures and activate inflammatory responses that underpin our ability to fight infectious disease. Many NLRs do so by forming molecular complexes called inflammasomes upon cellular infection with pathogenic bacteria, viruses and fungi. However, these innate immune responses can also be triggered in uninfected people by cell damage or metabolic stress, leading to diseases such cancer, gout and diabetes.

Our research focuses on understanding how immune cells launch healthy inflammation to fight infection and unhealthy inflammation to promote disease. By understanding exactly how the body fights infection, we can help identify new drug targets or vaccines to combat infectious disease, which causes 13 million deaths globally each year. By understanding how unhealthy inflammation is initiated, we may also be able to design new strategies for the treatment of common diseases such as cancer, gout and diabetes.



More details about our research

Inflammasomes provide a molecular platform for cluster-dependent activation of the protease, caspase-1, and thereby elicit a proteolytic signalling pathway that triggers the processing and secretion of proinflammatory mediators, and drives inflammatory cell death. These pathways culminate in immune system activation (inflammation), the induction of antimicrobial defence mechanisms, and microbial elimination. Inflammasomes can also be triggered by non-microbial structures (e.g. host molecules indicating cell stress or injury) and can thereby drive unhealthy inflammation in human disease. Genetic mutations in 8 NLR family members are associated with human heritable inflammatory disorders, and recent studies have identified an unexpected role for inflammasome-dependent cytokines in driving the inflammatory component of numerous chronic diseases (e.g. gout, diabetes, Alzheimer's disease).

During the past 12 months, we have made significant progress toward understanding the molecular mechanisms regulating inflammasome activation, and the cell types critical for inflammasome-mediated host defence and disease. Our current research focuses on mechanisms of signal integration between inflammasomes and other innate immune pathways (e.g. TLRs), the molecular mechanisms governing inflammasome and caspase activation, the evolutionary biology of inflammasomes, and the cellular mediators of inflammasome-dependent inflammation. We integrate molecular and cell biology approaches with in vivo studies to gain a holistic understanding of inflammasome function during infection, and inflammasome dysfunction in human inflammatory disease.

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Research in the news

27 November 2014 - Scientists uncover new intelligence behind inflammatory disease - IMB News

12 November 2014 - Young researchers awarded UQ fellowships - IMB News

28 October 2014 - Young immunologist receives coverted award - IMB News

8 November 2013IMB researchers to investigate if cholesterol affects the immune system - IMB News

31 October 2013 - Inflammation: A complex problem - Nature

17 September 2013 - Awards recognise UQ's rising stars of research - UQ News

21 June 2012Diabetes and sugarcane research at IMB receives a boost - IMB News

Research training opportunities

Expressions of interest from prospective postgraduate students are welcome at any time. For information on future research higher degree projects, please email Dr Kate Schroder with the following: (1) CV, including a summary of academic qualifications, work and research experience, and publication list; (2) studies report for undergraduate and honours degree(s); and (3) a letter of motivation outlining your research interests.

Please see IMB's postgraduate website for more information. 

Key publications

View more publications by Dr Schroder via PubMed, Google Scholar, or UQ Researchers.

Coll, R.C., Robertson, A.A., Chae, J.J., Higgins, S.C., Munoz-Planillo, R., Inserra, M.C., Vetter, I., Dungan, L.S., Monks, B.G., Stutz, A., Croker, D.E., Butler, M.S., Haneklaus, M., Sutton, C.E., Nunez, G., Latz, E., Kastner, D.L., Mills, K.H., Masters, S.L., Schroder, K., Cooper, M.A., O'Neill, L.A. (2015). A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases. Nature Medicine 21, 248-255.

Chen K.W., Groß C.J., Sotomayor F.V., Stacey K.J., Tschopp J., Sweet M.J., and Schroder K. (2014). The Neutrophil NLRC4 Inflammasome Selectively Promotes IL-1beta Maturation without Pyroptosis during Acute Salmonella Challenge. Cell Reports 8 (2): 570-82.

Schroder, K., Irvine, K.M., Taylor, M.S., Bokil, N.J., Le Cao, K.A., Masterman, K.A., Labzin, L.I., Semple, C.A., Kapetanovic, R., Fairbairn, L., Akalin, A., Faulkner, G.J., Baillie, J.K., Gongora, M., Daub, C.O., Kawaji, H., McLachlan, G.J., Goldman, N., Grimmond, S.M., Carninci, P., Suzuki, H., Hayashizaki, Y., Lenhard, B., Hume, D.A., and Sweet, M.J. (2012). Conservation and divergence in Toll-like receptor 4-regulated gene expression in primary human versus mouse macrophages. Proceedings of the National Academy of Sciences U S A 109 (16), E944-E953.

Schroder, K., Sagulenko, V., Zamoshnikova, A., Richards, A.A., Cridland, J.A., Irvine, K.M., Stacey, K.J., and Sweet, M.J. (2012). Acute lipopolysaccharide priming boosts inflammasome activation independently of inflammasome sensor induction. Immunobiology 217, 1325-1329.

Schroder, K., and Tschopp, J. (2010). The inflammasomes. Cell 140, 821-832.

Schroder, K., Zhou, R., and Tschopp, J. (2010). The NLRP3 inflammasome: a sensor for metabolic danger? Science 327, 296-300.

Tschopp, J., and Schroder, K. (2010). NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production? Nature Reviews Immunology 10: 210-215.


Group contacts

Dr Jelena Bezbradica
Research staff
+61 7 334 62351
+61 7 334 62356
Ms Jennifer Dou
Research staff
+61 7 334 62172
Dr Mercedes Monteleone
Research staff
+61 7 334 62356
Mr Damien Bierschenk
Research higher degree student
+61 7 334 62100
Dr Rebecca Coll
Research staff
+61 7 334 62356
Dr Kate Schroder
Group leader
+61 7 334 62058
+61 7 334 62351

Dr Dave Boucher
Research staff
FRSQ Postdoctoral Fellow
+61 7 334 62351 
+61 7 334 62356

Ms Kylie Georgas
Administrative assistant (part time)
Mrs Alina Zamoshnikova
Research higher degree student
+61 7 334 62351
+61 7 334 62356
Dr Kaiwen Chen
Research staff
+61 7 334 62071
+61 7 334 62087
+61 7 334 62351
Ms Caroline Holley
Research assistant
+61 7 334 62351