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Pattern Recognition Receptors In Inflammation And Infection
Funder
National Health and Medical Research Council
Funding Amount
$622,655.00
Summary
Innate immunity provides our first line of defence against infections, but pathogens can overcome this system. Understanding how microbes disable innate immunity can teach us how to prevent and/or treat infectious diseases. Innate immunity acts by initiating inflammation. Many important acute and chronic diseases develop when this process is dysregulated. Blocking innate immunity thus has potential to treat many diseases. This project aims to understand innate immunity in these contexts.
Reprogramming Innate Immunity To Combat Inflammatory And Infectious Diseases
Funder
National Health and Medical Research Council
Funding Amount
$1,788,220.00
Summary
Our immune system protects us from infection, but also drives cancer, autoimmune diseases, inflammatory diseases and many other conditions. Innate immunity, a key component of our immune system, mediates the pathology that is associated with these diseases. This research program aims to define innate immune mechanisms that combat infection and/or drive inflammation-mediated diseases. It also aims to deliver novel anti-infective and anti-inflammatory strategies.
Neuronal Toll-like 2 Receptors Contribute To The Spread Of Parkinson's Disease
Funder
National Health and Medical Research Council
Funding Amount
$900,010.00
Summary
How the pathological protein in Parkinson’s disease (PD), ?-synuclein, spreads through the brain remains unknown. Toll-like receptor 2 (TLR2) located on microglial cells have been identified as the receptor responsible for the internalization of ?-synuclein by this cell. We have found TLR2 in PD neurons accumulating Lewy pathologies, suggesting that neuronal TLR2 contributes to the neuronal spread of ?-synuclein in PD, a theory requiring further biological evidence prior to therapeutic targeting
The Role Of Toll Like Receptors In Leukocyte Activation And Adherence In Glomeruli In Auto-immune Glomerulonephritis
Funder
National Health and Medical Research Council
Funding Amount
$82,554.00
Summary
1 in 7 Australians have Kidney disease. Kidney disease tends to be progressive and over 8500 Australians require renal replacement therapy (dialysis). The cost of dialysis from 2004-2010 in Australia will be $ 4.5 billion. Auto-immune disease and Diabetes accounts for nearly 60% of kidney failure. Whilst current regimes exist to treat Kidney disease these are limited because they are deleterious side-effects. Improved understanding of the mechanism of disease will lead to improved treatments.
Consequences Of MYD88 Mutations Commonly Found In Human B Cell Malignancies
Funder
National Health and Medical Research Council
Funding Amount
$442,583.00
Summary
MYD88 is one of the most recurrently mutated genes in B cell malignancies, such as diffuse-large B cell lymphoma and Waldenström macroglobulinemia. This project will characterise oncogenic MYD88 mutations by introducing the mutations into normal mouse B cells. It will examine how the mutations disrupt signalling pathways and B cell functions and how the mutations respond to new lymphoma drugs. We hope this project will provide information for lymphoma pathogenesis and rational drug selection.
Mammalian Endotoxin: Characterisation Of Highly Inflammatory Endogenous Material
Funder
National Health and Medical Research Council
Funding Amount
$915,859.00
Summary
Inflammation drives development of many common diseases including heart disease, cancer, Alzheimer's disease and diabetes. We understand how bacterial molecules initiate inflammation during infections, but the nature of inflammatory stimuli that promote degenerative diseases of ageing has been elusive. In this project we will identify highly inflammatory molecules that have become altered in cells under stress. Knowledge of these pathways will promote new treatments for chronic diseases.
Excess inflammation is a major problem after injury and in many diseases. Upon injury molecules are release that act as danger signals to alert the immune system to start the repair process. However, high levels of these dangers signals can impair the final stages of healing. Understanding how to prevent the immune system being excessively stimulated by these danger signals is key to being able to dampen inflammation after injury improve the healing response.