How cell death affects your health

By Rob Clancy, staff writer. Reviewed by Associate Professor Kate Lawlor

Associate Professor Kate Lawlor researching Cell death and your health
Associate Professor Kate Lawlor

Associate Professor Kate Lawlor knows better than most that it is not death itself but how and when it happens that is most significant. A/Prof Lawlor leads the Cell Death and Inflammatory Signalling Group that investigates the intricate links between cell death and inflammation and how these processes impact various inflammatory and infectious diseases. She knows that when it comes to cell death – an essential and inevitable process – too much or too little is a problem: both are bad for your health.

Diseases linked to cell death

“Life is pleasant. Death is peaceful. It’s the transition that’s troublesome.” Isaac Asimov, American author and Professor of Biochemistry.

When cell death goes wrong, such as cells failing to die or dying at the wrong time, it can lead to many diseases including cancer, autoimmune diseases and neurodegenerative disorders, such as Alzheimer’s and Parkinson’s.

Cell death also regulates the body’s inflammatory response to infection and, when in excess, can drive both acute and chronic inflammatory conditions, such as sepsis, rheumatoid arthritis and type 2 diabetes.

How is cell death linked to better health?

A/Prof Lawlor explains that cell death is the removal of dead cells from the body to maintain healthy tissues and organs:

“It occurs in two ways, through natural controlled cell death (apoptosis), or through accidental cell death (necrosis) due to an injury or infection which can cause inflammation.

Mitochondria
Mitochondria

My team aims to understand how cell death regulates innate inflammatory responses, where innate immune cells act as the first line of defence against microbial infections and tissue injury.

“By understanding how cell death signalling coordinates inflammatory responses and tissue repair, we believe that we can selectively target cell death regulatory molecules to promote better health outcomes in a wide range of disorders.

“While activating cell death can be good in infection, too much cell death can drive tissue damaging inflammation, known as sepsis. Likewise, we have shown that elevated cell death directly triggers inflammation in acute and chronic inflammatory diseases, so my lab is trying to discover molecules that limit cell death and diminish inflammation,” she said.

Uncovering clues for therapeutics

2023 saw significant progress in this field, with research published in Cell Death & Disease and EMBO Reports that uncovered essential cell death regulatory molecules that dictate when specific innate immune cells die during normal ageing and to select bacterial infections. These achievements led the group to receive funding from the ARC to explore new areas of innate immune cell regulation.

For A/Prof Lawlor, this work brings multiple benefits:

“I enjoy that in my area of fundamental cell death research I get to dissect complex molecular pathways using innovative new technologies. But I am more excited by the fact that my findings have the potential to uncover new therapeutic targets that can be translated into the clinic to treat inflammatory disorders, infections and even cancer.

“Beyond this, my Research Group Head role has allowed me to inspire the next generation of medical researchers to have successful careers in both academia and industry.

“It’s a career that aims to deliver better treatments and incredible science, in a research area promising huge benefits for us all,” she said.

Collaborators | Monash University; Doherty Institute; WEHI

This research was supported by | ARC (Future Fellowship); NHMRC Ideas Grant

Journal | Cell Death and Disease

Title | RIPK3 controls MAIT cell accumulation during development but not during infection

View publication | https://doi.org/10.1038/s41419-023-05619-0

Journal | EMBO Reports

Title | A1 is induced by pathogen ligands to limit myeloid cell death and NLRP3 inflammasome activation

View publication | https://www.embopress.org/doi/full/10.15252/embr.202356865

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