Stained sites of inflammation
The Inflammation division seeks to understand the complex series of biological and molecular mechanisms that regulate inflammation.
Our aim is to improve the diagnosis, treatment and prevention of human inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, sepsis and rheumatic fever.

Discovering drivers of inflammation

Changes to our DNA can cause immune disorders by activating – or inactivating – genes that drive unwanted inflammatory responses, causing immune cells to inappropriately attack our own tissues.

Dr Man Lyang Kim, Associate Professor Seth Masters and colleagues identified the cellular pathway by which mutations in the gene Wdr1 trigger inflammation. Loss of Wdr1 causes the build-up of a critical cell structural protein called actin, which is inappropriately recognised by the immune sensor protein Pyrin, triggering inflammation. 

This discovery has implications for diagnosing and treating chronic inflammatory diseases and infections that alter actin dynamics.

Biomarkers for acute rheumatic fever and rheumatic heart disease

Rheumatic heart disease is a serious heart condition that results from complications of acute rheumatic fever (ARF), a disease that can follow bacterial infection. Rheumatic fever and heart disease are highly prevalent in Australia’s Aboriginal and Torres Strait Islander community, and a significant cause of early death.

Dr Willy-John Martin and Professor Ian Wicks are working to improve the diagnosis and treatment of ARF, and hopefully avoid long-term cardiac complications. They have identified novel biomarkers and an existing drug that modulates the immune system, which may hold potential for diagnosing and treating ARF.

Unravelling the causes of inflammation

The cell signalling molecule interleukin-1β (IL-1β) has a central role in promoting the inflammation that underlies conditions such as rheumatoid arthritis. There are several molecular pathways identified as producers of IL-1β, each of which may contribute to inflammation.

Dr Kate Lawlor, Dr James Vince and colleagues have revealed a previously unrecognised way that a protein called RIPK3 contributes to IL-1β production. RIPK3 had been thought to contribute to inflammation through its role in a form of cell death caused necroptosis. 

The team’s discovery that RIPK3 could drive IL-1β production without necroptosis may influence the design of new classes of anti-inflammatory drugs.

Health impact

Cancers: bowel cancer, breast cancer, melanoma, myeloproliferative disorders, pancreatic cancer, stomach cancer

Immune disorders: inflammatory bowel disease, lupus, psoriasis, rheumatic fever and heart disease, rheumatoid arthritis, sepsis

Infectious disease: chronic infections, influenza, vaccines

Division head

Professor Ian Wicks

Lab heads

Associate Professor Seth Masters

Associate Professor Sandra Nicholson

Dr James Vince

Dr Tracy Putoczki

Division coordinator

Dr Emma Prato