Understanding The Host Pathogen Relationships Of Hendra Virus In Bats, Horses And Humans
Funder
National Health and Medical Research Council
Funding Amount
$648,339.00
Summary
We will examine why bats can be infected with Hendra Virus with no apparent symptoms, yet the virus causes severe disease in other mammals including humans. We will examine the innate immune response towards the virus in the natural host (fruit bats), horses and humans. In addition to the innate immune response we will also examine the adaptive immune response in bats and humans. We hope this information can be used to design new drugs or vaccines to Hendra Virus.
An Investigation Into The Molecular Basis Of MAIT Cell Recognition Of Vitamin B Based Metabolites
Funder
National Health and Medical Research Council
Funding Amount
$883,762.00
Summary
Mucosal associated invariant T cells (MAIT cells) are an abundant T-cell population in humans, that is found mostly in the gastrointestinal mucosa. We have recently shown that MAIT cells can be activated by metabolites of vitamin B. This proposal will investigate how the MAIT cells "see" vitamin B metabolites. This research will pave the way for novel therapeutics that can modulate MAIT cell activity.
Argonaute Proteins In The Mammalian Antiviral Response
Funder
National Health and Medical Research Council
Summary
Viruses are the most abundant infectious agents on earth, and the diseases caused by them are a constant threat and cause of mortality worldwide. Awarded the Nobel Prize for Medicine in 2006, RNA interference (RNAi) is a natural process that plants use to attack viruses. Humans possess all of the tools for RNAi, but whether it is used for antiviral defense is unknown. This study aims to uncover this immune process which will open new avenues to treat virus infections, such as influenza and HIV.
Understanding The Role Of MAIT Cells In Health And Disease
Funder
National Health and Medical Research Council
Funding Amount
$547,593.00
Summary
A specialised set of T lymphocytes called Mucosal Associated Invariant T (MAIT) cells protect us from bacteria and yeast at mucosal sites where the body's immune defences are most easily breached, e.g. gut, oral cavity, airways & reproductive tract. This study investigates the role of MAIT cells in health and in diseases like inflammatory bowel disease, peptic ulceration, periodontitis and tuberculosis. Controlling MAIT cells could help in treating these conditions.
The Inflammasome In Host Defence And Autoinflammation
Funder
National Health and Medical Research Council
Funding Amount
$408,388.00
Summary
Inflammation is one of the bodies first responses to infection. The inflammasome is a protein complex that activates pro-inflammatory cytokines as part of this process. We are investigating pathogens that activate a specific inflammasome complex, and also an inflammatory disease it may cause when activated accidentally, in the absence of infection. We are also investigating pathways that keep this inflammation in check, and how pathogens might hijack these anti-inflammatory pathways to promote i ....Inflammation is one of the bodies first responses to infection. The inflammasome is a protein complex that activates pro-inflammatory cytokines as part of this process. We are investigating pathogens that activate a specific inflammasome complex, and also an inflammatory disease it may cause when activated accidentally, in the absence of infection. We are also investigating pathways that keep this inflammation in check, and how pathogens might hijack these anti-inflammatory pathways to promote infection.Read moreRead less
Recognition And Interaction Of Virus By The Innate Immune System
Funder
National Health and Medical Research Council
Funding Amount
$307,946.00
Summary
The innate immune system acts rapidly to limit infection of invading pathogens. The interaction and recognition of pathogens such as viruses by the innate immune system, is of importance to understand why particular pathogens induce disease.
TOLL LIKE RECEPTORS AGGRAVATE GLOMERULONEPHRITIS AND KIDNEY INJURY IN RENAL VASCULITIS
Funder
National Health and Medical Research Council
Funding Amount
$110,068.00
Summary
Anti neutrophil cytoplasmic antibody associated vasculitis (AAV) is a significant cause of morbidity and mortality. My thesis will explore the role of Toll Like Receptor (TLR) 2 and TLR9 in the initiation and pathogenesis of AAV and the therapeutic potential of TLR2/9 inhibitors. I will use both a murine experimental model and human kidney biopsy samples in this work. My thesis will further define the critical molecular events that underlie the disease whilst addressing potential new therapies.
Structural And Functional Characterisation Of The Killer Cell Immunoglobulin-like Receptor (KIR) Family Of Natural Killer Cell Receptors
Funder
National Health and Medical Research Council
Funding Amount
$348,070.00
Summary
Natural Killer (NK) cells are an important component of the immune response to cancer and infection. This project will define the molecular targets that are recognised by NK cells. This knowledge can then be used to guide in the selection of bone marrow donors in the treatment of leukemias as well as understanding how we fight off infections.
Inflammasome Function In Protection Against Infectious Disease And Autoimmunity
Funder
National Health and Medical Research Council
Funding Amount
$631,010.00
Summary
Inflammation, characterised by swelling, heat, pain and redness, is a normal response to injury and infection. Many human diseases such as gout, athersclerosis, diabetes and Alzheimer’s disease involve some inflammation, mediated through a common pathway termed the inflammasome. This project will investigate the proteins involved in this pathway and how they interact in their normal role of combatting infections, as well as a possible defect in this pathway in autoimmune patients.
PB1-F2 Is Critical To Influenza A Virus Pathogenicity Through Activation Of The Inflammasome
Funder
National Health and Medical Research Council
Funding Amount
$663,919.00
Summary
Fatal Influenza A virus infections are excessive inflammation. We identified the IAV protein PB1-F2 as critical in driving excessive inflammation via activating the host inflammasome complex. Our study evaluates PB1-F2-mediated inflammation contribution to inflammatory responses. Identifying PB1-F2 in emerging IAV strains is invaluable in aiding health policy makers to quickly assess fatal IAV pandemics. Our research will potentially identify treatment targets towards reducing this inflammation