The Australian Research Data Commons (ARDC) invites you to participate in a short survey about your
interaction with the ARDC and use of our national research infrastructure and services. The survey will take
approximately 5 minutes and is anonymous. It’s open to anyone who uses our digital research infrastructure
services including Reasearch Link Australia.
We will use the information you provide to improve the national research infrastructure and services we
deliver and to report on user satisfaction to the Australian Government’s National Collaborative Research
Infrastructure Strategy (NCRIS) program.
Please take a few minutes to provide your input. The survey closes COB Friday 29 May 2026.
Complete the 5 min survey now by clicking on the link below.
Structural Basis Of Influenza A Virus-specific CD8+ T Cell Receptor Diversity
Funder
National Health and Medical Research Council
Funding Amount
$469,500.00
Summary
Viral infection results in the activation and proliferation of virus-specific T cells that mediate clearance of virally infected cells. Recognition of virally infected cells is meditated by presentation of peptide fragments complexed to Major histocompatibility complex (MHC) class I glycoproteins. Virus-specific T cells recognise these viral protein fragments via a specific receptor expressed at the T cell surface. This proposal plans to examine the structural factors that determine influenza-sp ....Viral infection results in the activation and proliferation of virus-specific T cells that mediate clearance of virally infected cells. Recognition of virally infected cells is meditated by presentation of peptide fragments complexed to Major histocompatibility complex (MHC) class I glycoproteins. Virus-specific T cells recognise these viral protein fragments via a specific receptor expressed at the T cell surface. This proposal plans to examine the structural factors that determine influenza-specific T cell receptor recognition. From these studies, we plan to determine how these structural factors can influence the diversity of virus-specific T cells that are generated after viral infection. The conclusions from these studies will enable us to determine why some virus-specific T cell responses are not diverse and what are the consequences for virus-specific T cell immunity. This has implications for the development of novel vaccine strategies designed to induce immunity against both viral and tumour challenge.Read moreRead less
Chromatin Remodelling And Transcriptional Regulation Of CD8 T Cell Effector Gene Expression
Funder
National Health and Medical Research Council
Funding Amount
$531,696.00
Summary
A major role for cytotoxic, or killer, T cells is the recognition and removal of virus infected or tumor cells from a host. Upon recognition of a target host cell, killer T cells deliver a package of proteins, termed granzymes, that mediate the removal of these virus infected and tumor cells. Naive killer T cells need to be activated to start producing these effector molecules. This proposal plans to examine the factors that regulate both induction and maintanence of cell specific expression of ....A major role for cytotoxic, or killer, T cells is the recognition and removal of virus infected or tumor cells from a host. Upon recognition of a target host cell, killer T cells deliver a package of proteins, termed granzymes, that mediate the removal of these virus infected and tumor cells. Naive killer T cells need to be activated to start producing these effector molecules. This proposal plans to examine the factors that regulate both induction and maintanence of cell specific expression of these effector molecules. We plan to identify the molecular events that occur within a cells genome to turn on granzyme gene expression and how these factors influence subsequent killer T cell function. The conclusions from these studies will enable us to determine why some killer T cell responses are not effective and what can be done to improve killer T cell function. This has implications for the development of novel vaccine strategies designed to induce immunity against both viral and tumour challenges.Read moreRead less
Regulation Of TNF And SFK Signalling In Immune Cells By TCPTP
Funder
National Health and Medical Research Council
Funding Amount
$454,023.00
Summary
Tumour necrosis factor (TNF) is a potent proinflammatory cytokine that plays an important role in immunity and inflammation. TNF acts on the cell surface to activate two key cellular communication or signalling pathways: the mitogen-activated protein kinase (MAPK) pathway and the nuclear factor kappaB (NFkappaB) pathway. The relative activation of the two pathways can dictate whether cells live and proliferate or differentiate or otherwise die in response to TNF, and therefore determine the natu ....Tumour necrosis factor (TNF) is a potent proinflammatory cytokine that plays an important role in immunity and inflammation. TNF acts on the cell surface to activate two key cellular communication or signalling pathways: the mitogen-activated protein kinase (MAPK) pathway and the nuclear factor kappaB (NFkappaB) pathway. The relative activation of the two pathways can dictate whether cells live and proliferate or differentiate or otherwise die in response to TNF, and therefore determine the nature of the immune or inflammatory response. The T-cell protein tyrosine phosphatase (TCPTP) is known to be important in the immune system and serves as a negative regulator of inflammation. Our preliminary studies have identified TCPTP as a selective regulator of TNF-induced MAPK but not NFkappaB signaling. TCPTP exerts its effects by inactivating Src family kinases (SFK) which are themselves integral to immune and inflammatory responses. In this proposal we will elucidate the molecular basis for TCPTP function in TNF- signalling and characterise the role of TCPTP in TNF and SFK functions in immune cells, in particular T-cells.Read moreRead less
HIV currently infects ~40 million people world-wide, causing ~3 million deaths in 2003, mainly in the world's poorest countries. A cheap, effective vaccine seems the best means of preventing the spread of the epidemic. The two main approaches to vaccination are either to make antibodies (which bind to and inactivate the virus), or killer T cells (which kill infected cells). Many of these vaccines are now being tested in monkeys. The results of killer T cell vaccination trials have been both enco ....HIV currently infects ~40 million people world-wide, causing ~3 million deaths in 2003, mainly in the world's poorest countries. A cheap, effective vaccine seems the best means of preventing the spread of the epidemic. The two main approaches to vaccination are either to make antibodies (which bind to and inactivate the virus), or killer T cells (which kill infected cells). Many of these vaccines are now being tested in monkeys. The results of killer T cell vaccination trials have been both encouraging and disappointing. The vaccines do not appear able to prevent the monkeys from getting infected with the virus. However, in many cases even though the monkeys become infected with HIV, they do not get the usual disease associated with AIDS, and hence live with rather than die from this infection. The aims of this project are to use statistical analysis, and more complex mathematical and computer models to try to analyse the data generated by these vaccine trials and to understand how these partially effective vaccines help control virus. For example, even if a vaccine does not prevent infection, we can investigate whether it slowed viral growth, or increased killing of infected cells, and if so, whether an increase in this response could be effective. In preliminary work we have analysed data from a vaccination trial performed in Boston. The results of this study suggest that the reason vaccinated monkeys still become infected is that the killer T cells produced by the vaccine do not appear to activate for the first 10 days of infection. In these first 10 days the virus grows normally and is able to establish a foothold for continuing infection. By contrast, we find that antibodies act extremely early after infection. The methods we propose have not been used before to study vaccines, and by studying the kinetics of the virus and immune response from a large number of vaccine trials we hope to help identify the optimal vaccine design.Read moreRead less
I am an Immunologist interested in the role of B-lymphocytes, their survival and expression of a novel chemoreceptor in Autoimmunity. I also study the important role of Neuropeptide Y in modulating key immune functions.