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Field of Research : Autoimmunity
Research Topic : VESTIBULAR DISEASE
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  • Funded Activity

    Cellular Pathogenesis Of Key Proteins Involved In Neurodegenerative Disorders

    Funder
    National Health and Medical Research Council
    Funding Amount
    $312,730.00
    Summary
    Prion proteins are involved in neurodegenerative diseases such as Creutzfeldt-Jakob disease (CJD) and Bovine Spongiform Encephalopathy (BSE). The aim of this research proposal is to investigate factors which can change the prion protein from a normal, benign, form into an abnormal shape which can cause disease. The outcomes of this work will provide further insight into the role of prion proteins in these diseases and also for other neurodegenerative disorders such as Alzheimer's disease.
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    Funded Activity

    Genetic Characterisation Of Factors Involved In Regulating The Production Of Autoantibodies

    Funder
    National Health and Medical Research Council
    Funding Amount
    $313,004.00
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    Funded Activity

    The Associations Of Mutations Linked To Familial Forms Of Transmissible Spongiform Encephalopathy Diseases

    Funder
    National Health and Medical Research Council
    Funding Amount
    $208,108.00
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    Funded Activity

    Investigations In Multiple Sclerosis Patients With Coexistent Autoimmune Thyroid Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $557,100.00
    Summary
    Multiple sclerosis (MS) is a common chronic neurological disease affecting over one million people around the world. MS is generally thought to be an autoimmune disease, in which a person's own immune cells start to attack components of the brain and spinal cord. However, it is thought that the same components are not attacked in all patients, and that the pathway that leads to MS varies from one person to another. Therefore, in order to develop successful treatment strategies for MS, it will be .... Multiple sclerosis (MS) is a common chronic neurological disease affecting over one million people around the world. MS is generally thought to be an autoimmune disease, in which a person's own immune cells start to attack components of the brain and spinal cord. However, it is thought that the same components are not attacked in all patients, and that the pathway that leads to MS varies from one person to another. Therefore, in order to develop successful treatment strategies for MS, it will be necessary to look for patterns in the clinical symptoms and signs and other features of a person's MS that may give clues as to which particular pathway is leading to disease in that person. Some people who develop MS also develop other autoimmune diseases, or have these other diseases before they develop MS, or have other family members who have other autoimmune diseases. We have recently found that people who have the same combination of coexistent MS and autoimmune thyroid disease (AITD) show similar clinical signs of MS, and tend to have damage (lesions) to the same areas of their nervous system. This suggests that these people may have the same underlying pathways leading to the development of MS, and that they may be a very informative group in which to look for immune or genetic abnormalities that might explain why they develop MS. This project will investigate people who have both MS and AITD and other members of their families to see if we can work out what the links are between having the same combination of autoimmune diseases and developing lesions in particular parts of the nervous system. It will provide information on the pathways that lead to the development of MS, and information obtained from this study may eventually be of use in developing more specific therapeutic agents, by tailoring therapies to specific people with MS, depending on the clinical and immunological profile of that person.
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    Funded Activity

    The Influence Of NF-KB In The Development Of Autoimmunity And Cancer In Fas/FasL Mutant Mice

    Funder
    National Health and Medical Research Council
    Funding Amount
    $596,925.00
    Summary
    Apoptotic cell death is an essential process in the human body, it removes useless and dangerous cells, preventing autoimmune disease and cancer. Apoptosis is activated when the surface receptor Fas is stimulated by its ligand, FasL, but defective signalling causes disease associated with deregulated NF-?B activation. We will investigate how faulty FasL-induced apoptosis cooperates with deregulated NF-kB activation or defective Aire (immunological tolerance orchestrator) results in autoimmunity.
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    Funded Activity

    The Role Of Susceptibility Genes And Microbiota In Inflammatory Diseases

    Funder
    National Health and Medical Research Council
    Funding Amount
    $303,924.00
    Summary
    Utilising my background in Immunology I will investigate whether specific genetic mutations can create a susceptibility for dysregulation of the flora and immune system within the gut, thus predisposing an individual to inflammatory bowel diseases (ulcerative colitis and Crohn's disease) as well as non-intestinal inflammatory conditions. These diseases are becoming an increasingly prevalent and serious health burden in Australia. We aim to use this knowledge in order to design specific treatment .... Utilising my background in Immunology I will investigate whether specific genetic mutations can create a susceptibility for dysregulation of the flora and immune system within the gut, thus predisposing an individual to inflammatory bowel diseases (ulcerative colitis and Crohn's disease) as well as non-intestinal inflammatory conditions. These diseases are becoming an increasingly prevalent and serious health burden in Australia. We aim to use this knowledge in order to design specific treatments for these diseases.
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    Funded Activity

    Thymic Epithelial Cell Apoptosis, Aire And Autoimmune Disease.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $470,799.00
    Summary
    Autoimmune diseases, like diabetes and multiple sclerosis are a significant disease burden. Their root cause is the failure of the immune system to distinguish between the body's own tissues and potential pathogens. We propose to study how potentially dangerous immune cells are destroyed in the thymus before they can develop. This research will significantly improve our understanding of how autoimmune diseases begin.
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    Funded Activity

    Molecular Signatures Of Public Clonotypes In Human Systemic Autoimmunity

    Funder
    National Health and Medical Research Council
    Funding Amount
    $540,633.00
    Summary
    New platform technology has been developed to study autoantibody clones in lupus and Sjogren's syndrome. This approach has furthered our understanding of these disorders by the discovery of unique sets of clones that are common to all patients. The unique "molecular signatures" of these clones can be translated to a next-generation diagnostic that detects them in patients at extremely low levels missed by conventional tests.
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    Funded Activity

    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.
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    Funded Activity

    In Vivo Investigation Of Human PR3 Transgenic Mice: A Novel Animal Model To Understand The Role Of PR3 In Chronic Inflammation And Autoimmune Vasculitis

    Funder
    National Health and Medical Research Council
    Funding Amount
    $378,615.00
    Summary
    Granulomatosis with polyangiitis (GPA) is a form of vasculitis and is associated with antibodies directed against proteinase 3 (PR3). PR3 is expressed in neutrophils, monocytes and macrophages and has a number of well-characterized pro-inflammatory functions. The aim of this project is to understand the role of PR3 in inflammation and autoimmune vasculitis in vivo. This will be achieved using a transgenic mouse model expressing human PR3.
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