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Congrats Wael, Jia Jia and Jamie on securing NHMRC Investigator Grants

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Monash BDI researchers secure more than $18M in NHMRC Investigator Grants

Nine researchers from the Monash Biomedicine Discovery Institute (BDI) have secured more than $18 million in funding through the National Health and Medical Research Council’s (NHMRC) 2026 Investigator Grant scheme, announced by Federal Minister for Health and Ageing, Mark Butler.

 

Monash BDI’s NHMRC Investigator Grants 2026 recipients: Prof Mary Herbert, Prof Jamie Rossjohn, Prof Andrew Ellisdon, A/Prof Rhys Grinter, Prof Francine Marques, Dr Wael Awad,  Dr Lauren Alesi, Dr Meiling Han, Dr Jia Jia Lim.

Professor Dena Lyras, Interim Director of the Monash BDI, said the funding highlights the strength and diversity of the Institute’s research community.

“These Investigator Grants support some of Australia’s most innovative and ambitious biomedical research programs, and I’m delighted to see nine Monash BDI researchers recognised through this highly competitive scheme,” Professor Lyras said.

“The funded projects span a remarkable breadth of research, from reproductive health and cardiovascular disease to cancer immunotherapy, antimicrobial resistance and AI-enabled drug discovery. Together, they have the potential to deliver important advances in our understanding of disease and contribute to the development of new treatments that improve health outcomes,” she said.

“This funding will enable our researchers to pursue bold ideas and address some of the most significant health challenges facing Australia and the global community. I congratulate all of our Investigator Grant recipients on this achievement and acknowledge the significant effort that goes into developing applications for such a competitive funding scheme.”

The nine Monash BDI projects are among 26 projects awarded more than $49 million in funding to Monash Medicine Nursing and Health Sciences (MNHS) researchers in the latest NHMRC Investigator Grants. Read more on each of the MNHS recipients here.

The Rossjohn lab researchers to receive funding were:

Professor Jamie Rossjohn FAA FRS, A molecular investigation into T cell antigen receptor function and dysfunction in humans

T cells play a key role in the human immune system. However, there are many aspects of T cell mediated immunity we do not understand. This proposal is focused on understanding the molecular mechanisms underpinning how T cell antigen receptor (TCR) recognition events govern cellular immunity in the context of protective, aberrant and anti-tumour immunity. This includes understanding how TCRs recognise peptides, lipids and metabolites presented by the MHC, CD1 and MR1 family of antigen presenting molecules.

Emerging Leadership 2

Dr Wael Awad, Harnessing Cancer-Activated Invariant T cells for next-generation cancer immunotherapy

A newly discovered cancer-fighting immune cell could pave the way for next-generation immunotherapies that work across a wide range of tumour types. This project focuses on cancer-associated invariant T (CAIT) cells, which recognise cancer-related metabolic signals presented by the molecule MR1. Using structural biology, biochemistry and immunology, this project aims to identify the tumour metabolites that activate these cells and develop novel MR1-based therapies. The findings could reveal universal cancer targets and support the creation of broadly applicable immunotherapies and vaccines for cancer treatment and prevention.

Emerging Leadership 1

Dr Jia Jia Lim, Targeting CD1a-restricted T cells for molecular intervention in skin autoimmunity  

New insights into how the skin’s immune system responds to altered lipids, with the goal of  developing more targeted treatments for inflammatory skin diseases. This project focuses on CD1a, an immune molecule that presents lipid antigens to T cells and can trigger harmful immune responses when skin lipids are altered by factors such as UV exposure or cosmetic products. Using structural biology and immunology, the research will uncover how altered lipids activate pathogenic T cells and explore ways to block these interactions, providing a foundation for improved therapies for psoriasis, eczema and allergic contact dermatitis.

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Congrats Mohamed on your first authored JEM paper

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Scientists discover natural molecules that help calm immune cells

First author on the JEM publication, Monash BDI PhD student Mohamed Abdelaal, and co-senior and co-corresponding author, Dr. Wael Awad.

Researchers have uncovered a surprising way the human body helps keep its immune system in check. The study found that when the body breaks down vitamin B2 (riboflavin), it produces natural molecules that can reduce the activity of MAIT cells – specialised immune cells involved in inflammation.

Co-led by Monash Biomedicine Discovery Institute (BDI) and University of Melbourne researchers, and published in the Journal of Experimental Medicine, the discovery shows that our bodies naturally produce molecules that can suppress MAIT cell activity, filling a major gap in understanding how the body maintains immune balance. Previously, research focused on how bacteria activate these cells, but little was known about the body’s own regulatory mechanisms.

These molecules interact with an immune sensor called MR1, which normally helps activate MAIT cells. Instead of boosting MR1 activity like vitamin-related molecules do, the body’s own molecules keep MR1 inside the cell, lowering its presence on the surface and dampening the immune response.

“Our findings reveal a natural mechanism that prevents unnecessary immune activation and inflammation,” said Mohamed Abdelaal, a PhD student with the Monash BDI and first author of the study.

“Understanding this process opens the door to new ways of controlling inflammation and immune-related diseases, by targeting overactive immune responses,” he said.

The study highlights a new dimension of MR1 biology and its role in immune homeostasis, paving the way for future research into how metabolic byproducts influence immunity.

Next steps include testing these molecules in living systems and exploring drug-like compounds that fine-tune MAIT cell activity, potentially leading to new therapeutic targets for immune disorders.

This study was co-led by Dr Wael Awad from Monash University’s Biomedicine Discovery Institute, and Dr Nicholas Gheradin from the Peter Doherty Institute for Infection and Immunity, University of Melbourne.

Read the full paper published in the Journal of Experimental Medicine, titled The antigen presenting molecule MR1 binds host-generated riboflavin catabolites.
DOI: 10.1084/jem.20250711

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Where there is smoke …. there is fire – Congrats to co-first author Wael

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Researchers discover how cigarette smoke impairs critical lung immune cells

Cigarette smoking is widespread and deadly, yet our understanding of how cigarette smoke actually causes serious respiratory illnesses in incomplete, which has severely hampered the development of effective treatments. In the Journal of Experimental Medicine (JEM) Australian researchers reveal how multiple chemicals found in cigarette smoke and e-cigarettes alter the function of a key type of immune cell found in the lungs.

The study suggests that these alterations make cigarette smokers, and those exposed to second- and third-hand smoke, more susceptible to respiratory infections, and exacerbate smoking-related inflammatory diseases such as chronic obstructive pulmonary disease (COPD).

Cigarette smoking is known to impair the immune system’s response to infections and promote inflammation in the lungs that can lead to or exacerbate COPD, the third leading cause of death worldwide. COPD patients are more susceptible to influenza infections that can, in turn, exacerbate the underlying disease by increasing airway inflammation and promoting the destruction of the lung’s air sacs. There are currently no effective treatments for COPD.

According to Dr Wael Awad, from Monash University’s Biomedicine Discovery Institute, until now the mechanisms underlying the skewed immune responses in people exposed to cigarette smoke, and how they are related to smoke-associated diseases like COPD remain unclear,” says Dr Awad, first author on the new JEM study.

Professor Jamie Rossjohn of Monash University’s Biomedicine Discovery Institute co-led the study with Professor David P. Fairlie of the Institute for Molecular Bioscience at University of Queensland, Professor Alexandra J. Corbett of the University of Melbourne, based at the Peter Doherty Institute for Infection and Immunity, and Professor Philip M. Hansbro of the Centenary Institute and University of Technology Sydney.

In their study, the researchers looked at the effects of cigarette smoke on Mucosal-Associated Invariant T (MAIT) cells, a type of immune cell found in the lungs and other tissues of the body. MAIT cells help fight off bacterial and viral infections and can promote inflammation or tissue repair.

MAIT cells are activated by a protein called MR1 that is found in almost every cell of the body. MR1 recognizes chemicals produced by bacteria and presents them at the surface of infected cells in order to activate MAIT cells and initiate an immune response. “We suspected that some of the more than 20,000 chemicals present in cigarette smoke that smokers inhale might also bind to MR1 and influence the activity of MAIT cells in the lungs”, Dr Awad said.

The researchers used computer modeling to predict which components of cigarette smoke might be recognized by MR1 and then found that several of these molecules not only bound to the protein but also either increased or decreased in amounts on the surface of cells. These chemicals, including benzaldehyde derivatives that are also used as flavorings in e-cigarettes, blocked activation of human MAIT cells by compounds produced by bacteria.

Unveiling the Molecular Impact of Smoking on Lung Health. This illustration explores how smoke components in cigarette and e-cigarette smoke obscures critical chemicals that bind MR1 and disrupt T cell functions in the lungs. Image: Erica Tandori

The research team then studied the effects of cigarette smoke on MAIT cells from human blood and mice and showed they reduced MAIT cell function. Mice repeatedly exposed to cigarette smoke developed symptoms of lung disease and this was worsened if also infected by influenza. Researchers found that long-term exposure to cigarette smoke altered the protection provided to mice by their MAIT cells, making them less able to fight off influenza infections and more prone to the development of COPD disease.

“We found that mice lacking MAIT cells were also protected from cigarette smoke-induced COPD, showing reduced levels of lung inflammation and no tissue deterioration in their lung’s air sacs” Profesor Hansbro said.  “This study demonstrates the power of collaboration and the insights we can gain with inter-disciplinary science,” Professor Corbett said.

“Overall, our study reveals that components of cigarette smoke can bind to the protein MR1 and reduce the functions of protective immune cells called MAIT cells. This increases susceptibility to infections worsens progression of lung disease” Awad says. The researchers now plan to investigate exactly which MAIT cell pathways are impacted by cigarette smoke, in order to learn how to better treat COPD and other lung diseases.

Read the full paper in Journal of Experimental Medicine: Cigarette smoke components modulate the MR1-MAIT axis. DOI: 10.1084/jem.20240896

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Monash study unravels another piece of the puzzle in how cancer cells may be targeted by the immune system

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Effective immunity hinges on the ability to sense infection and cellular transformation. In humans, there is a specialised molecule on the surface of cells termed MR1. MR1 allows sensing of certain small molecule metabolites derived from cellular and microbial sources; however, the breadth of metabolite sensing is unclear.

Published in PNAS, researchers at the Monash University Biomedicine Discovery Institute (BDI) have identified a form of Vitamin B6 bound to MR1 as a means of engaging tumour-reactive immune cells. The work involved an international collaborative team co-led by researchers from the University of Melbourne.

 

Monash BDI authors on the study (L-R): Dr Patricia Illing, Dr Wael Awad, Dr Mitchell McInerney .

Monash BDI authors on the study (L-R): Dr Patricia Illing, Dr Wael Awad, Dr Mitchell McInerney .

According to Dr Illing, “Our findings suggest that Vitamin B6 molecules displayed by MR1 represent a means for the immune system to detect altered cellular metabolism/metabolite levels that may distinguish cancer cells,” she said.

“Identification of small molecules/metabolites able to activate immune cells with cancer reactivity is a key step in understanding how small molecule sensing might contribute to anti-cancer immunity.”

Central to this study were the unbiased mass spectrometry analysis of small molecules bound to MR1, the structural resolution of the interactions between MR1 and Vitamin B6, and immunological assays performed by lead authors Dr Mitchell McInerney and Dr Wael Awad at Monash Biomedicine Discovery Institute, and Dr Michael Souter and Mr Yang Kang at the University of Melbourne, Peter Doherty Institute.

While it’s not yet clear if the Vitamin B6 molecule can be utilised in therapeutics, “understanding the breadth of MR1 mediated immunity has the capacity to illuminate routes for therapeutic intervention,” Dr Illing said.

An important aspect of the finding is that MR1 differs very little across individuals – with few known genetic variants in the human population. “Thus, understanding immune activation mediated via MR1 may pave the way for therapeutic interventions with broad utility,” Dr Illing said.

She added that next steps for investigation will confirm whether Vitamin B6 and related molecules are displayed by the MR1 of cancer cells at altered levels to healthy body cells, thus enabling specific cancer targeting, or if other small molecules displayed by MR1 may help differentiate cancerous and healthy cells.

Read the full paper published in PNAS, titled MR1 presents vitamin B6–related compounds for recognition by MR1-reactive T cells
DOI: 10.1073/pnas.2414792121

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Congrats to our newly appointed BDI Group Leaders: Wael, Jan and Adam

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Monash BDI announce new Group Leaders

Monash Biomedicine Discovery Institute (BDI) is excited to announce 13 newly selected Group Leaders. These Group Leaders are part of a program created by Monash BDI to help early career researchers (ECRs) bridge the gap between senior postdoctoral fellow and independent lab head.

Professor Dena Lyras, Deputy Director at the Monash BDI, said that this program provides recognition and additional career momentum for researchers who are leading novel, cutting-edge research programs and developing their independence.

“Congratulations to all of the newly selected Group Leaders. This is a testament to the hard work and dedication of these researchers, and we look forward to seeing their next steps and achievements,” said Professor Lyras.

Congratulations to the newly selected Monash BDI Group Leaders:

Dr Wael Awad seeks to elucidate the mechanistic basis underpinning metabolite capture and loading of the MHC class I-related molecule “MR1” by cellular chaperones, by using cutting-edge molecular, immunological and biochemical approaches. He also explores the scope of environmental and microbial metabolites that can modulate human T cell immunity. Such studies pave the way for the development of innovative therapeutics based on selective modulation of T cell immunity.

Dr Jan Petersen’s research focuses on antimicrobial immunity and natural killer (NK) cell immunity. He investigates how T cells and NK cells recognise microbial peptide antigens presented by major histocompatibility complex (MHC) molecules, and aims to decipher the molecular mechanisms that define the ability of the adaptive immune system to distinguish between self and foreign. Focused on events central to infection and immunity, his work is aimed at understanding outcomes in various diseases and transplantation.

Dr Adam Shahine is focused on the molecular roles of lipids in the regulation and dysregulation of human adaptive immunity. Using structural biology, he seeks to investigate the mechanisms of lipid antigen recycling, and the presentation of lipid antigens by CD1 antigen presenting molecule family T cells.

Dr Deepak Adhikari aims to gain a better understanding of how mitochondria are formed and how they regulate the development of eggs and offspring.

Dr Asolina Braun aims to understand what initially causes psoriasis and hence to discover new treatments for this skin disease. Her research is focused on finding peptides that trigger and set off the detrimental immune response in psoriasis.

Dr Luke Formosa investigates how mitochondrial enzymes are built from their individual subunits, and how this process is disrupted in mitochondrial disease. One in 5,000 children will develop a mitochondrial disease, but about one-third of patients won’t have a genetic diagnosis. By discovering new genes that play a role in this process, the diagnosis of patients can be improved, paving the way for new treatments for this disease.

Dr Meiling Han’s research targets antibiotic resistance, focusing on the mechanism(s) underpinning the extensive membrane remodelling that occurs in Gram-negative bacteria and the interactions between remodelled bacterial membranes and membrane-targeting antimicrobials (e.g. lipopeptides). The fundamental mechanistic information that she generates will greatly inform the future design of much-needed antibiotics against antibiotic-resistant bacteria.

Dr Anja Knaupp’s research centres on characterising cell-type-specific sets of proteins and determining how they operate. Insight into these molecular mechanisms and drivers is key for our understanding of cellular identity and changes that, for example, occur during cancer development.

Dr Rachael Lappan aims to understand the nature and basis of microbial life in the atmosphere, the largest but most unexplored potential ecosystem on Earth. Using cutting-edge molecular and biogeochemical approaches, she aims to identify true microbial residents of the atmosphere, understand their mechanisms for survival in this environment and explore their role in seeding newly formed environments.

Dr Kate McArthur’s research uses a variety of microscopy and cell biology techniques to understand the mechanisms behind, and immune responses to, mitochondrial changes and aberrant cell death during disease.

Dr Nitin Patil is investigating peptide- and oligonucleotide-based antimicrobial drug development and delivery.

Dr Francesca Short combines genomic and molecular microbiology approaches to understand bacterial behaviour and adaptation. Her current research focuses on how bacteria control the production of virulence factors during infection and on how common disinfectants can compromise antibiotic efficacy.

Dr Yogitha Srikhanta investigates strategies that bacterial gut pathogens employ to proliferate, cause disease and survive, with a focus on antibiotic resistance and epigenetic-mediated gene regulation.

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