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Monocyte Chemotactic Protein-1 (MCP1) And The PTH Anabolic Effect In Bone.
Funder
National Health and Medical Research Council
Funding Amount
$690,435.00
Summary
Chemokines and their receptors are major regulators of cell-cell interactions in many tissues. This project explores the strong increase of monocyte chemotactic protein-1 (MCP1 or CCL2) in bone, in a treatment where parathyroid hormone (a controller of calcium homeostasis) is used to increase bone mass to prevent osteoporosis. MCP1 was previously thought to be an inflammatory regulator, induced during infection and important in autoimmune conditions, so its role in bone was highly unexpected.
Role of antibodies and their receptors in chronic inflammation: The activation of inflammatory white blood cells is a major mechanism of tissue destruction in certain autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. It is well known that destructive chemicals, enzymes and hormones are released by these cells into affected tissues, for example joints and kidneys. What is lacking is knowledge of the earliest steps in the immune system that activate the inflammator ....Role of antibodies and their receptors in chronic inflammation: The activation of inflammatory white blood cells is a major mechanism of tissue destruction in certain autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. It is well known that destructive chemicals, enzymes and hormones are released by these cells into affected tissues, for example joints and kidneys. What is lacking is knowledge of the earliest steps in the immune system that activate the inflammatory white blood cells and drive this inflammation cascade to the point where chemicals are released and tissued destroyed. This project investigates the role of one of the major receptor families involved in the activation of inflammation. These are receptors for antibodies called FcR. The binding to these receptors of unusual antibodies produced in autoimmune disease initiate events that stimulate white blood cells leading to their activation and the secretion of inflammatory substances. Our work leading up to this project has been very exciting and has shown that one receptor in particular, FcgammaRIIa is unique to humans, is the most widespread FcR in the body and is the most potent activator of inflammatory substance release. We will be studying animal models to precisely define how this human receptor works. Mice have been generated which contain this uniquely human receptor and these mice develop many features of human autoimmune disease such as the joint destruction, kidney destruction and lung destruction seen in both rheumatoid arthritis and lupus. The principal aim of our study is to define the role of this human receptor in the development of inflammatory conditions with the ultimate goal of using this information to generate new treatments for these diseases.Read moreRead less
The Design, Development And Clinical Assessment Of A New Metacarpophalangeal Joint Prosthesis
Funder
National Health and Medical Research Council
Funding Amount
$188,450.00
Summary
Rheumatoid arthritis is a crippling form of arthritis that affects many people in the community. It commonly involves the finger joints in the hands resulting in deformity, pain and subsequent loss of function. There have been implants designed for finger joint replacement, but unfortunately these implants have had only moderate benefits and can break and lead to further joint destruction resulting in the worsening of deformity and pain. A new implant for finger joint replacement has been develo ....Rheumatoid arthritis is a crippling form of arthritis that affects many people in the community. It commonly involves the finger joints in the hands resulting in deformity, pain and subsequent loss of function. There have been implants designed for finger joint replacement, but unfortunately these implants have had only moderate benefits and can break and lead to further joint destruction resulting in the worsening of deformity and pain. A new implant for finger joint replacement has been developed. This implant has several potential advantages. Firstly the unique design acts to prevent recurring deformity in the fingers with rheumatoid disease while allowing functional motion. Secondly, it is thought that patients will return to function earlier and avoid the need for further finger surgery as this implant design relies less on the tissues around it for stability. The purpose of this study is to investigate the biomechanical and clinical benefits of this new implant for finger joint replacement. The new design will undergo specific laboratory tests and be used in a clinical trial to quantify the therapeutic benefits it provides to patients with rheumatoid arthritis.Read moreRead less
The Role Of Fc RIIa In Antibody Dependent Tissue Destruction In Autoimmunity
Funder
National Health and Medical Research Council
Funding Amount
$538,206.00
Summary
These studies will attempt to identify the cause autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus we are using a unique strain of mice carrying a unique human protein called Fc receptor that triggers inflammatory cells. We will identify the processes that start inflammation, and those that continue throughout chronic autoimmune disease. These studies will be applied to the development of new treatments for autoimmune disease.
Structure And Function Of Receptors For IgG (FcgammaR)
Funder
National Health and Medical Research Council
Funding Amount
$748,500.00
Summary
How FcR function in normal and destructive immunity: This research project is studying one of the most important receptor families of inflammatory white blood cells known in immunology. These receptors called Fc Receptors (FcR) bind complexes of specialised proteins called antibodies with foreign antigens, i.e. bacteria, viruses, called immune complexes. As a direct consequence of this binding, a chain of events in inflammatory white blood cells is set in motion, leading to the destruction of fo ....How FcR function in normal and destructive immunity: This research project is studying one of the most important receptor families of inflammatory white blood cells known in immunology. These receptors called Fc Receptors (FcR) bind complexes of specialised proteins called antibodies with foreign antigens, i.e. bacteria, viruses, called immune complexes. As a direct consequence of this binding, a chain of events in inflammatory white blood cells is set in motion, leading to the destruction of foreign pathogens, however in autoimmune diseases this same processes leads to the severe inflammation causing destruction of joints in rheumatoid arthritis and kidneys in glomerulonephritis or allergies, bleeding disorders. Our studies are aimed at understanding the very first events that initiate this inflammatory cascade, i.e. how immune complexes bind to FcR and having bound these, how these receptors are organised to initiate the inflammatory cascade. Our studies will use new techniques such as X-ray crystallography to take 3D photographs of FcR interacting with immune complexes and genetic engineering studies to validate our 3D photographs. If we understand how immune complexes bind to FcR and how the receptors are organised on the cell membrane, we will be able to apply this information to the development of new treatments that either interfere with immune complex binding or receptor organisation. Although these concepts are well established in other fields e.g. growth hormone receptors, very little is known about the organisation of receptors involved directly in immunity. These novel studies will provide us with powerfully useful insights into the first steps in antibody driven tissue destruction.Read moreRead less
Structure And Function Of Receptors For IgG (FcgammaR)
Funder
National Health and Medical Research Council
Funding Amount
$905,280.00
Summary
This reasearch project is attempting to understand one of the most important mechanisms of resistance to infectious disease and one of the most important mechanisms of induction of destructive inflammation in autoimmune disease. These studies will define how blood proteins called antibodies, antibodies bind to the surface of white blood cells via proteins called Fc receptors that activate these white blood cells. Under normal circumstances this system provides resistance to infection but is invo ....This reasearch project is attempting to understand one of the most important mechanisms of resistance to infectious disease and one of the most important mechanisms of induction of destructive inflammation in autoimmune disease. These studies will define how blood proteins called antibodies, antibodies bind to the surface of white blood cells via proteins called Fc receptors that activate these white blood cells. Under normal circumstances this system provides resistance to infection but is involved in some of the most debilitating diseases, including allergies, bleeding disorders called thrombocytopoenias, inflammation of blood vessels, vasculitis, as well as aspects of rheumatoid arthritis. The successful conclusion of this project will result in knowledge that will enable the development of more effective and highly specific therapeutic approaches to the treatment of disease and a better understanding of the functioning of the immune system.Read moreRead less
Novel Mechanisms And Targets In Neonatal Lupus: Clues To Systemic Autoimmunity
Funder
National Health and Medical Research Council
Funding Amount
$428,250.00
Summary
Autoimmune diseases represent the third greatest clinical burden to the community after heart disease and cancer. Management of the diseases remains primitive because of our poor understanding of the disease mechanisms. Autoantibodies are one of the key markers of diseases such as lupus and Sj gren's syndrome, but their role in producing tissue damage is largely unresolved. However in the neonatal lupus syndrome, autoantibodies from the mothers cross the placenta and appear to cause inflammation ....Autoimmune diseases represent the third greatest clinical burden to the community after heart disease and cancer. Management of the diseases remains primitive because of our poor understanding of the disease mechanisms. Autoantibodies are one of the key markers of diseases such as lupus and Sj gren's syndrome, but their role in producing tissue damage is largely unresolved. However in the neonatal lupus syndrome, autoantibodies from the mothers cross the placenta and appear to cause inflammation of particular target organs such as the heart and skin in the babies. Neonatal lupus offers a unique opportunity to investigate the pathological role of autoantibodies and other factors (e.g. infection) in autoimmune diseases, and is likely to offer vital clues to lupus in adults. For example, the skin disease in babies with lupus mimics the cutaneous lesions in adult lupus patients. Recent work from our group using an animal model has shown that certain autoantibodies cross the placenta and bind to cells undergoing physiological death in the fetus, in the same organ distribution as human neonatal lupus. Using sophisticated imaging techniqes we can now trace the fate of maternal autoantibodies in the babies for the first time and understand how the target proteins in heart and skin become exposed to the damaging effects of these autoantibodies. We also believe that certain types of autoantibodies can directly alter contraction and electrical activity in the heart in babies with neonatal lupus, leading to heart block which can be fatal. We have already discovered similar functional autoantibodies in adult patients with Sj gren's syndome whose babies can also also develop neonatal lupus, and plan to characterise them using unique physiological assays in intact hearts. We will characterise the redistribution of antigenic proteins in cells in fetuses and the interaction of maternal autoantibodies with these proteins to cause tissue damage and functional heart block.Read moreRead less
The Role Of Suppressor Of Cytokine Signalling-3 (SOCS-3) In Chondrocytes During Development And Disease
Funder
National Health and Medical Research Council
Funding Amount
$348,392.00
Summary
Cytokines are messenger proteins produced and secreted from one cell which then bind to specific receptors on the surface of other cells. After binding, a series of intracellular events occurs, termed signalling, that results in the target cell changing its behaviour. Cytokine signalling, if allowed to proceed unchecked, can result in various disease states. The suppressor of cytokine signalling (SOCS) proteins are key negative regulators of cytokine signalling within the cell. They are induced ....Cytokines are messenger proteins produced and secreted from one cell which then bind to specific receptors on the surface of other cells. After binding, a series of intracellular events occurs, termed signalling, that results in the target cell changing its behaviour. Cytokine signalling, if allowed to proceed unchecked, can result in various disease states. The suppressor of cytokine signalling (SOCS) proteins are key negative regulators of cytokine signalling within the cell. They are induced by a wide range of stimuli, especially from a group called the IL-6 family. We have preliminary data showing that cartilage cells (chondrocytes) normally produce a particular SOCS protein, called SOCS-3. We have also shown that when SOCS-3 production is dysregulated, the chondrocytes undergo excessive proliferation. Normal chondrocyte function is important during skeletal development and diseases such as osteoarthritis are thought to result from abnormal chondrocyte behaviour. It is likely that SOCS-3 has a key role in regulating chondrocyte function. The aim of this proposal is therefore to examine the role of SOCS-3 in chondrocytes, during development and in disease. Much of our understanding of the role of the SOCS proteins comes from the construction of mutant mice that lack a particular SOCS protein. When mutant mice are made that lack SOCS-3 in the whole animal the mice die before birth and so virtually nothing is known about the role of SOCS-3 in chondrocytes and the implications for cartilage in disease states, such as arthritis. To answer this we will create mice that lack SOCS-3 specifically in their chondrocytes. Evaluating the role of SOCS-3 in cartilage development and chondrocyte function during degenerative and inflammatory disease states is potentially of major clinical importance in improving our understanding of arthritis and of cartilage repair.Read moreRead less
Defining The Role Of GILZ In Inflammatory Arthritis
Funder
National Health and Medical Research Council
Funding Amount
$675,030.00
Summary
Corticosteroids are commonly used to treat inflammatory diseases such as arthritis. Their action is based on effects on natural inflammation control pathways. One such pathway is that mediated by the protein known as GILZ (glucocorticoid induced leucine zipper). The function of this protein in disease is not well understood, and the research proposed here will increase understanding of its role. This knowledge could yield new treatments for arthritis and other inflammatory diseases.