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Inflammatory diseases, such as autoimmune diseases, result from an overactive immune system. A new therapy that is currently under trial is the use of special blood cells, called Treg cells, whose function is to suppress unwanted immune responses. This application evaluates the efficacy and safety of such treatments.
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.
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.
How Deletional And Non-Deletional Tolerance Mechanisms Integrate To Prevent Autoimmune Disease
Funder
National Health and Medical Research Council
Funding Amount
$509,944.00
Summary
The body produces millions of immune cells every day to fight infection. Some of these immune cells are defective and dangerous because they can cause autoimmune diseases, like Type I diabetes and multiple sclerosis. To defuse this risk, such immune cells are either caused to die or are inactivated to prevent autoimmunity. We propose to investigate how the processes of immune cell death and inactivation work in health and disease so we may harness these mechanisms to cure autoimmunity.
How Does NF-kB2 Regulate Thymic Selection To Prevent Organ-specific Autoimmune Disease?
Funder
National Health and Medical Research Council
Funding Amount
$787,600.00
Summary
Autoimmune diseases like type 1 diabetes and thyroiditis arise from defects that cause the immune system to confuse self and non-self. Normally, this distinction is programmed in the thymus. We recently identified the gene that causes a form of autoimmune disease. We also made an important discovery about how the thymus gland regulates self-non-self discrimination. We will build on these two discoveries to gain a precise understanding of how the immune system normally avoids autoimmune disease.
Dendritic Cells And CCAAT/enhancer Binding Protein-delta (CEBP?) In Neuroinflammation And Autoimmunity
Funder
National Health and Medical Research Council
Funding Amount
$576,538.00
Summary
This projects aims to develop new treatments by finding the cells and chemicals that naturally stop inflammation in the central nervous system in diseases like MS. It also aims to test new treatments by delivering them to where this inflammation takes place. This targeted delivery should mean fewer side effects because the rest of the body is not exposed to the treatment. Hopefully this will reduce the impact of these diseases on the community, and reduce side effects for the patient.
The Role Of NF-?B Transcription Factor RelA In Regulatory T Cell Homeostasis And Function
Funder
National Health and Medical Research Council
Funding Amount
$637,114.00
Summary
Treg cells constitute an immune regulatory cell population that is essential for the prevention of fatal autoimmunity; however, they also limit immunity against cancer. We have discovered that the factor RelA is of critical importance for Treg development and function. We now aim to illuminate the functions of RelA in detail. Understanding the molecules that impact on Treg cell biology is critical to harness their potential for clinical intervention such as treatment of autoimmunity and cancer.
A Novel Role For The IL-2 Pathway In Type-1-diabetes.
Funder
National Health and Medical Research Council
Funding Amount
$548,548.00
Summary
Genes encoding IL-2 and its receptor are strongly linked to susceptibility to multiple autoimmune diseases, including type-1-diabetes. Despite the importance of this pathway in the immune system, it is not yet understood how the associated genes affect disease. In this study, a novel function for IL-2 expression by dendritic cells in normal self-tolerance is investigated. The impacts of dendritic cell produced IL-2 expression and linkage to autoimmunity will be elucidated in both mouse and man.
How Does Genetic Variation For Trig Affect Autoimmune Responses Mediated By Toll-like Receptors?
Funder
National Health and Medical Research Council
Funding Amount
$671,114.00
Summary
Juvenile diabetes is an autoimmune disease that affects more than 120,000 Australians. We have recently discovered a novel gene, named Trig, in a genetic study of mice that develop juvenile diabetes similar to children. This research proposal aims to determine the function of Trig in the immune system and how it contributes to the development of autoimmune diseases, such as juvenile diabetes.
The Molecular Basis Of Human CD4+ T-cell Responses In Autoimmune Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$656,498.00
Summary
Over 120,000 Australians currently suffer from type 1 diabetes. This incurable disease typically strikes in childhood or adolescence and is caused by the immune system destroying the cells which make insulin. This project aims to determine how and why the insulin producing cells are recognized by the immune system. Eventually this work will lead to new vacccines to prevent the immune system from destroying the insulin producing cells.