Investigations Into The Aetiology Of Giant Cell Arteritis
Funder
National Health and Medical Research Council
Funding Amount
$165,067.00
Summary
Despite much research the precise pathoetiology of giant cell arteritis is poorly understood. Both environmental and genetic factors are thought to contribute to disease development. Though to date, no overriding mechanism for disease development has been identified. This research will apply modern molecular techniques to further explore the pathogenic processes in this devastating disease which in turn will hopefully provide insight into novel treatment modalities.
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.
How The Kidney Is Injured By CD8+ Cells In Vasculitis
Funder
National Health and Medical Research Council
Funding Amount
$928,780.00
Summary
People with severe kidney disease often have inflammation in the small blood vessels within their kidneys, known as vasculitis. Human observational studies suggest that a type of immune cell, the CD8+ cell, may be critical to disease outcome, but there is no functional evidence for this. The current studies will define the role of these CD8+ cells in disease so that better treatments for humans with vasculitis can be considered.
Therapeutic Blockade Of Complement Inducing Inflammatory Injury In Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$133,181.00
Summary
ANCA associated vasculitis is an inflammatory disease involving the kidney filters which is a major cause of chronic kidney failure. Current drugs to treat it are toxic. Less toxic treatments are required. In this study we will explore the potential for new treatments targeting complement (a normal blood protein involved in inflammation) to attenuate this disease in mice. We hope to define the role of complement in this disease and the benefits of inhibiting it before we use it in humans.
Targeting The Inflammasome To Treat ANCA Associated Glomerulonephritis
Funder
National Health and Medical Research Council
Funding Amount
$122,686.00
Summary
Anti neutrophil cytoplasmic antibody (ANCA) vasculitis is a type of kidney disease which causes significant morbidity and mortality in the Australian population. Current treatments are toxic and are associated with significant side-effects. This research focusses on a pathway of immune activation which is of emerging importance, called the inflammasome, which may be a target for future therapies in this disease.
The Pathogenesis Of PR3-ANCA Associated Vasculitis
Funder
National Health and Medical Research Council
Funding Amount
$128,224.00
Summary
ANCA-associated vasculitis (AAV) is a rare but severe cause of autoimmune renal disease, which can lead to renal failure and death. Our research and understanding of AAV until now has been largely limited to MPO-AAV. This proposal provides a unique opportunity to further understand PR3-AAV by utilising a new mouse model of the disease. This knowledge will inform further research regarding therapeutic targets, thereby improving care of patients affected by PR3-AAV.
Plasma Exchange And Glucocorticoids In Anti-neutrophil Cytoplasm Antibody Associated Systemic Vasculitis: A Randomised Controlled Trial (PEXIVAS Australia)
Funder
National Health and Medical Research Council
Funding Amount
$420,110.00
Summary
ANCA-associated vasculitis is a life-threatening disease. The PEXIVAS trial will investigate whether plasma exchange, in addition to immunosuppressive therapy and glucocorticoids, will reduce death and the development of severe kidney failure due to this disease. Additionally, the project will also look at whether using a reduced dose of glucocorticoids is just as effective as larger doses in lessening the infectious complications of treatment.