Immunological Studies Of Adjutant Induced Arthritis
Funder
National Health and Medical Research Council
Funding Amount
$412,104.00
Summary
This project stems from our interest in rheumatoid arthritis and a number of other forms of arthritis that affect many joints in a symmetrical fashion (the polyarthritides). In most instances, there is evidence that the diseases are caused by an attack on the joint lining (the synovium) by cells of the immune system. Rheumatoid arthriis is the most common and often the most severe of the polyarthritides. Neither the triggering event nor the target of the attack by the immune system is understood ....This project stems from our interest in rheumatoid arthritis and a number of other forms of arthritis that affect many joints in a symmetrical fashion (the polyarthritides). In most instances, there is evidence that the diseases are caused by an attack on the joint lining (the synovium) by cells of the immune system. Rheumatoid arthriis is the most common and often the most severe of the polyarthritides. Neither the triggering event nor the target of the attack by the immune system is understood and as a result, there are no specific preventative measures against the disease or specific therapies for the established disease. There is, however, strong evidence that the cells involved in the attack on the synovium are orchestrated by a white blood cell called the T lymphocyte. T lymphocytes cannot operate alone but require a second cell, the dendritic cell, to present the target in a special way which can be recognised and responded to by the T lymphocyte. The T cell and the dendritic cell are the two central aspects of this project. We will use an animal model of polyarthritis to allow access to these cells during the earliest phases of the disease, a silent period not recognisable in the earliest stages of rheumatoid arthritis. T lymphocytes from animals with experimental polyarthritis will be used as indicators in the search for the target of the disease process and dendritic cells from affected joints will be used as a natural source of that target. By the production of highly specific T lymphocytes (members of clones), we hope to identify the target molecules of the disease process. This information should lead ultimately to the identification of the triggering stimulus (and thence prevention) and to the development of highly specific therapies designed to treat the established disease.Read moreRead less
Studies On The Flavivirus Nonstructural Proteins And Untranslated Regions Of The Genome Involved In Virus Replication
Funder
National Health and Medical Research Council
Funding Amount
$244,277.00
Summary
Flaviviruses cause potentially fatal diseases of global importance such as yellow fever, Japanese encephalitis (JE) and dengue haemorrhagic fever. Flavivirus disease is also important in Australia with recurrent outbreaks of dengue fever, Australian encephalitis and more recently JE in the northern regions of the continent. Effective vaccines are only available to yellow fever and JE and tick-borne encephalitis and are either live or killed preparations which are potentially hazardous and costly ....Flaviviruses cause potentially fatal diseases of global importance such as yellow fever, Japanese encephalitis (JE) and dengue haemorrhagic fever. Flavivirus disease is also important in Australia with recurrent outbreaks of dengue fever, Australian encephalitis and more recently JE in the northern regions of the continent. Effective vaccines are only available to yellow fever and JE and tick-borne encephalitis and are either live or killed preparations which are potentially hazardous and costly to produce. There are no therapeutic agents (antivirals) available against flavivirus diseases. To produce safe and cost effective vaccines against flaviviruses and to identify targets for antiviral agents, a more complete understanding of how these viruses replicate in the cell and cause disease is required. This investigation aims to define specific aspects of the flavivirus life cycle that are currently unknown.Read moreRead less