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The Structural Basis Of T Cell Recognition In The Context Of Lipid Presentation And The CD1 Isoforms
Funder
National Health and Medical Research Council
Funding Amount
$380,558.00
Summary
CD1 molecules are critical in our host-defence against microbial pathogens. They survey our body for microbial lipids and then present them to our immune system for surveillance by T cell receptors. We aim to understand how a T cell receptor interacts with a CD1-lipid molecule. This interaction is crucial to the activation of our immune response and hence the elimination of the microbe. Once understood, this interaction can potentially be modified and has immunotherapeutic potential.
Mechanism Of Action, Homeostatic Role And Therapeutic Effects Of CD52
Funder
National Health and Medical Research Council
Funding Amount
$410,902.00
Summary
T cells are required to fight infections but sometimes attack our tissues and cause autoimmune disease. T cells called regulatory T (Treg) cells suppress other T cells that cause autoimmune disease. We discovered a new type of Treg cell that suppresses other T cells by releasing from its surface a protein called CD52. We aim to discover how CD52 works and show that it can prevent autoimmune disease. We will gain insight into how the immune system regulates itself and may identify a new drug for ....T cells are required to fight infections but sometimes attack our tissues and cause autoimmune disease. T cells called regulatory T (Treg) cells suppress other T cells that cause autoimmune disease. We discovered a new type of Treg cell that suppresses other T cells by releasing from its surface a protein called CD52. We aim to discover how CD52 works and show that it can prevent autoimmune disease. We will gain insight into how the immune system regulates itself and may identify a new drug for the treatment of autoimmune diseases.Read moreRead less
Evaluation Of Specificity, Mechanism Of Action And Therapeutic Use Of Peptides That Disrupt T-cell Antigen Receptor
Funder
National Health and Medical Research Council
Funding Amount
$166,885.00
Summary
Molecular disorganisation of receptor assembly renders the receptor incompetent and the cell unable to perform its normal function. In autoimmune diseases where the target is self the ability to stop autoreactive T cells is a therapy. Synthetic compounds known as peptides have been developed in our laboratory with the ability to disrupt cell function and we are at the forefront of such research. We hypothesise that if you prevent the receptor from assembling properly then it will not function. T ....Molecular disorganisation of receptor assembly renders the receptor incompetent and the cell unable to perform its normal function. In autoimmune diseases where the target is self the ability to stop autoreactive T cells is a therapy. Synthetic compounds known as peptides have been developed in our laboratory with the ability to disrupt cell function and we are at the forefront of such research. We hypothesise that if you prevent the receptor from assembling properly then it will not function. The end result is the potential to develop novel drugs with new means to treat inflammation in a number of autoimmune disorders including diabetes, rheumatoid arthritis, multiple sclerosis and psoriasis. Application of this concept is not restricted to immunology or the disruption of the T-cell antigen receptor but has wider therapeutic application to other multicomponent receptors relevant in the field of oncology, endocrinology, and allergy. By design one can produce peptides that will specifically inhibit specific cellular functions based on structure-function relationships. Further research into this area will then allow design of new non-peptide chemical entities based on the original peptide sequence and structure with easier pharmacological handling properties and efficacy. This project aims to define necessary features of the peptide and test it in humans.Read moreRead less
Identifying The Underlying Mechanisms Responsible For The Generation Of Pathogenic B Cells In Type 1 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$163,755.00
Summary
Type 1 diabetes (T1D) occurs when the body's own immune system mistakenly attacks and destroys all the beta cells of the pancreas which produce insulin, a hormone essential for regulating sugar levels in the blood. The non-obese diabetic (NOD) mouse develops a form of T1D closely resembling the human disease, and as a model, has led to numerous important insights into its cause. Based on studies in NOD mice, it is now well accepted that a class of cell in the immune system, termed T cells, are r ....Type 1 diabetes (T1D) occurs when the body's own immune system mistakenly attacks and destroys all the beta cells of the pancreas which produce insulin, a hormone essential for regulating sugar levels in the blood. The non-obese diabetic (NOD) mouse develops a form of T1D closely resembling the human disease, and as a model, has led to numerous important insights into its cause. Based on studies in NOD mice, it is now well accepted that a class of cell in the immune system, termed T cells, are responsible for most of the damage to the beta cells in T1D. Recent work in this model, however, has demonstrated that another class of immune cell, termed B cells, also play an important role in T1D as NOD mice made deficient in these cells no longer develop disease. In addition to producing antibodies, B cells are one of the few cell types which are able to take up and present protein fragments in a form recognizable to T cells. Normally, this only leads to the activation of T cells recognising foreign insults, like viruses or bacteria, resulting in their destruction. We have shown that a dangerous population of B cells can arise in NOD mice that can specifically take up beta cell proteins and present them to the T cells, which subsequently become armed to recognise and destroy the beta cells. Just like T cells, B cells that recognize the body's own proteins are normally eliminated in healthy mice and human individuals. This research proposal aims to determine the faulty immune mechanisms that give rise to the beta cell specific B cells in NOD mice. We have also set out to identify the diabetes susceptibility genes which control the generation of this dangerous population of B cells in this model. By understanding how these dangerous B cells are generated in NOD mice, we hope to form the basis for new therapies aimed at inhibiting these cells from forming in T1D susceptible humans, thus preventing the disease at an early stage.Read moreRead less
A Helminth-derived Peptide Is A Novel Prophylactic And Therapeutic Treatment For Autoimmune Disease
Funder
National Health and Medical Research Council
Funding Amount
$658,778.00
Summary
Parasitic worms (helminths) secrete molecules that possess a remarkable ability to skew the mammalian immune system towards anti-inflammatory responses. We have expoited a novel peptide secreted by helminths, which offers tremendous potential for the development of novel prophylactic and therapeutic treatments for a range of immune-mediated conditions. The overarching aim of this project is to further elucidate the mechanism of action and to determine the peptide’s clinical application.
Gestational diabetes is an important medical condition. We plan to investigate two subgroups of women with gestational diabetes. Firstly, women who have diabetes antibodies in pregnancy. Secondly, women who have a mild form of diabetes caused by a single gene mutation, who may be first identified during pregnancy. Correct identification of these subgroups of women is important for immediate and long-term management of both the mother and her fetus.
Cell-mediated Immune Responses In Cytomegalovirus-induced Myocarditis
Funder
National Health and Medical Research Council
Funding Amount
$238,407.00
Summary
The proposed research will provide a clearer understanding of the body's immune response to virus and self tissues in inflammatory heart disease. Inflammation of the heart, myocarditis, can occur following virus infection. The condition may be chronic and persist for a long time even after the virus infection has resolved. The autoimmune response attacks the body's own tissues and involves reactivity to a heart protein, namely myosin. Important immune cells (B and T cells) play a role in the dis ....The proposed research will provide a clearer understanding of the body's immune response to virus and self tissues in inflammatory heart disease. Inflammation of the heart, myocarditis, can occur following virus infection. The condition may be chronic and persist for a long time even after the virus infection has resolved. The autoimmune response attacks the body's own tissues and involves reactivity to a heart protein, namely myosin. Important immune cells (B and T cells) play a role in the disease process. Antibodies are produced by B cells during the virus infection which react to myosin but we do not know the reactivity of T cells in this disease. Natural molecules (cytokines) produced by our body are important for shaping our immune response (T and B cell-mediated) in virus infections and diseases. Autoimmune disease is a result of a mistake by our immune system. Such diseases can be triggered by virus infection and require immunotherapy for correction. In the project, we propose to : 1. Investigate immunological responses of immune cells (T cells) in the heart using an experimental mouse model of cardiovascular disease. 2. Examine the response of T cells to myosin using the mouse model of infection with a herpesvirus, cytomegalovirus (CMV). 3. Study the role of cytokines and immunotherapy in our CMV-triggered myocarditis model. Determination of the events leading to cardiovascular disease will allow developments of improved treatment and potential vaccinations against inflammatory heart disease. The findings from the proposed project are expected to have broader impact for other viruses invading the heart and their associated diseases in man.Read moreRead less
Organ-specific Autoimmunity: The Role Of The Thymus And Periphery In Shaping The Gastric-specific T Cell Repertoire
Funder
National Health and Medical Research Council
Funding Amount
$579,763.00
Summary
The immune system normally protects against invasion by pathogens such as harmful viruses and bacteria. In autoimmune diseases the same mechanisms that are used to protect us are erroneously targeted to our own tissues. White blood cells, called T lymphocytes are responsible for attacking our own tissues in autoimmune diseases. Our studies will employ a range of molecular, genetic and imaging technologies to track the rare and potential harmful white blood cells. Our studies should reveal the me ....The immune system normally protects against invasion by pathogens such as harmful viruses and bacteria. In autoimmune diseases the same mechanisms that are used to protect us are erroneously targeted to our own tissues. White blood cells, called T lymphocytes are responsible for attacking our own tissues in autoimmune diseases. Our studies will employ a range of molecular, genetic and imaging technologies to track the rare and potential harmful white blood cells. Our studies should reveal the mechanisms by which these self destructive T lymphocytes are silenced in healthy individuals on the one hand, and on the other hand escape to cause destruction in individuals with autoimmune diseases. This fundamental information will allow the development of therapeutic strategies to selectively turn-off these destructive T lymphoctyes in individuals with autoimmune disease and thereby remove the damaging immune response and cure the disease.Read moreRead less