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Personal profile

Biography

Dr Lawlor received her PhD in Medical Biology in 2004 at the Walter and Eliza Hall Institute of Medical Research and The University of Melbourne. After being awarded an NHMRC CJ Martin Overseas Biomedical Fellowship, she completed postdoctoral research at the Cambridge Institute for Medical Research, University of Cambridge, UK and the Walter and Eliza Hall Institute, most recently in the laboratory of Dr James Vince. During this time she established expertise in the molecular and cellular dissection of inflammatory signalling pathways, and the translation of these findings in vivo using models of autoimmune, inflammatory and infectious diseases. In 2018, she was recruited to head the Cell Death and Inflammatory Signalling group within the Centre for Innate Immunity and Infectious Diseases at the Hudson Institute.

Research interests

The Cell Death and Inflammatory Signalling group aims to identify new molecules that regulate cell death and inflammatory signalling.  We also seek to establish whether cell death signalling can be inhibited therapeutically to treat inflammatory disease, or triggered to promote antimicrobial responses.

Dr Lawlor and her team investigate the cross-talk between programmed cell death and inflammatory signalling pathways in disease. In particular, the laboratory studies how cell death induces activation of innate immune cell pattern recognition receptors (PRRs), including the inflammasomes. Inflammasomes are now known to activate pro-inflammatory protein Interleukin-1β (IL-1β) to induce a lytic form of cell death, called pyroptosis. This activity is critical for clearance of microbial organisms by the immune system. However, excess IL-1β activity can exacerbate rare hereditary autoinflammatory syndromes and common diseases, such as rheumatoid arthritis, type 2 diabetes and cancer.

External positions

Honorary Fellow, The Walter and Eliza Hall Institute of Medical Research (WEHI)

Research area keywords

  • innate immunity
  • Inflammasomes
  • Cell death
  • Inflammatory diseases
  • Signalling pathways
  • Infection and immunity
  • Autoimmune Diseases

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Projects 2018 2023

Research Output 2001 2019

Deleting Suppressor of Cytokine Signaling-3 in chondrocytes reduces bone growth by disrupting mitogen-activated protein kinase signaling

Liu, X., D'Cruz, A. A., Hansen, J., Croker, B. A., Lawlor, K. E., Sims, N. A. & Wicks, I. P., 5 Jun 2019, (Accepted/In press) In : Osteoarthritis and Cartilage. 7 p.

Research output: Contribution to journalArticleResearchpeer-review

Macrophages, rather than DCs, are responsible for inflammasome activity in the GM-CSF BMDC model

Erlich, Z., Shlomovitz, I., Edry-Botzer, L., Cohen, H., Frank, D., Wang, H., Lew, A. M., Lawlor, K. E., Zhan, Y., Vince, J. E. & Gerlic, M., Apr 2019, In : Nature Immunology. 20, 4, p. 397-406 10 p.

Research output: Contribution to journalLetterResearchpeer-review

Repurposing drugs targeting the P2X7 receptor to limit hyperinflammation and disease during influenza virus infection

Rosli, S., Kirby, F. J., Lawlor, K. E., Rainczuk, K., Drummond, G. R., Mansell, A. & Tate, M. D., Oct 2019, In : British Journal of Pharmacology. 176, 19, p. 3834-3844 11 p.

Research output: Contribution to journalArticleResearchpeer-review

Open Access
File

Stressing out the mitochondria: Mechanistic insights into NLRP3 inflammasome activation

Yabal, M., Calleja, D. J., Simpson, D. S. & Lawlor, K. E., Feb 2019, In : Journal of leukocyte biology. 105, 2, p. 377-399 23 p.

Research output: Contribution to journalReview ArticleResearchpeer-review

Sugar Fix Keeps RIPK3 at Bay

Giogha, C. & Lawlor, K. E., 19 Mar 2019, In : Immunity. 50, 3, p. 539-541 3 p.

Research output: Contribution to journalShort SurveyOtherpeer-review