Production Of Interferon Lambda By Dendritic Cell Subsets And Role In Adjuvant Effects Of Poly I:C
Funder
National Health and Medical Research Council
Funding Amount
$396,541.00
Summary
This proposal describes the identification of specific cells in mouse and humans that produce the anti-viral compound interferon-lambda. We propose to further characterise the mechanisms that induce interferon-lambda expression by these cell types and to decipher how this is controlled at the genetic level. We also aim to determine how the production of interferon lambda by these cell types can influence the immune response to viral infection.
The Role Of A Novel Cytokine Of The Innate Immune Response In Viral Infection
Funder
National Health and Medical Research Council
Funding Amount
$344,407.00
Summary
Sexually transmitted infections represent a critical global health and socioeconomic problem with over 1 billion new cases per annum. I propose a world-first description of a new protein that has a protective role against herpes simplex virus (HSV) infection of female reproductive tract. This unique protein, called interferon epsilon, was discovered in our laboratory. This project will facilitate development of new therapeutic approaches of benefit in HSV-2 infection.
Cytoplasmic DNA As A Danger Signal For Mammalian Cells
Funder
National Health and Medical Research Council
Funding Amount
$592,661.00
Summary
DNA in mammalian cells is contained within a structure known as the nucleus. The presence of DNA outside the nucleus in the cytoplasm of the cell is a sure sign that something is wrong, and may indicate the presence of a viral invader. In this case, the cell initiates anti-viral responses, including production of anti-viral proteins and death of the infected cell to stop replication of the virus. Lack of proper control of these responses may contibute to the autoimmune disease lupus.
Enhancing Host Defence Against Intracellular Pathogens By Preventing INOS Interaction With A Negative Regulator, SSB-2
Funder
National Health and Medical Research Council
Funding Amount
$448,881.00
Summary
Secretion of nitric oxide (NO) gas by immune cells is a critical defence mechanism for the killing of intracellular pathogens. Production of NO within cells is regulated by the enzyme iNOS. We propose that preventing iNOS from interacting with its natural inhibitor protein (SSB-2) would allow enhanced and prolonged iNOS expression leading to increased NO and increased killing of pathogens such as the mycobacterium tuberculosis and the Leishmania parasite.