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It is feasible to sequence patient genomes but we need to know more about how genetic variants cause complex disease. We have sequenced genomes from patients with immune deficiency and will test the idea that genetic variation causes consistent changes in particular white blood cells, thus providing a bridge between genomic information and clinical diagnosis. Outcomes will include more accurate diagnosis, better understanding of immunity, and a strategy for using whole genome information.
Applying Quantitative Immunology To The Analysis Of Complex Genetic Diseases
Funder
National Health and Medical Research Council
Funding Amount
$864,596.00
Summary
The immune response of each individual varies. For some, the response invoked by foreign challenge is weak, leading to a lifetime of difficulty with infection. For others, the response is stronger, yielding excellent immunity, but opening the potential for overactive responses to self-material and autoimmune disease. We have a new theory for how the health of our immune system can be measured and we aim to apply it to understand the genesis of the many different forms of human immune diseases.
HIV is one of the highest public health priorities of our time. Traditional vaccines have been unsuccessful highlighting the need for alternative approaches to HIV vaccine design. We propose to modify a novel technology developed initially for targeted drug delivery, termed “capsules”, for the purpose of inducing an immune response. This is a generic technology with applications for other infectious diseases and cancer and brings together disparate disciplines of nanochemistry and immunology.
The Mechanism For Combined Immunodeficiency And Autoimmunity Due To STK4-deficiency And Its Broader Application To Human PIDs
Funder
National Health and Medical Research Council
Funding Amount
$648,371.00
Summary
Why do some patients develop autoimmune diseases such as lupus where the immune system makes antibodies that attack its own body? To answer this, we plan to study a disease where a gene responsible for making antibodies is defective. Patients with mutations in the STK4 gene are unable to regulate the selection processes by which only the right cell is chosen to make antibodies. Understanding how STK4 works may help us unlock the mystery of what causes lupus.
Determining The Role Of DOCK8 In CD4+ T And B Cell Differentiation And Its Implications On Autosomal Recessive Hyper IgE Syndrome (AR-HIES)
Funder
National Health and Medical Research Council
Funding Amount
$512,600.00
Summary
Autosomal recessive hyper IgE (AR-HIES) syndrome due to mutations in DOCK8 is a rare primary immunodeficiency whereby patients present with susceptibility to severe and recurrent viral infections as well as an increased risk of developing cancer, severe food and environmental allergies, and atopic disease characterised by hyper IgE and extreme eosinophilia. This grant will investigate how abnormal DOCK8 function in CD4+ T cells and B cells contributes to disease pathogenesis in AR-HIES patients.
Utilising Human Primary Immunodeficiencies To Study Lymphocyte Differentiation
Funder
National Health and Medical Research Council
Funding Amount
$429,346.00
Summary
Human immunodeficiencies are diseases arising from naturally occurring mutations. In this instance, the specific genes mutated in the immunodeficiencies we study have been identified. However, it is unclear how defects in these genes make an individual manifest as an immune deficient state, rendering them vulnerable to disease. By studying immune cells from these individuals we hope to uncover the normal function of these genes and subsequently provide for new therapies for these conditions.
Mechanisms That Control Epstein Barr Virus Infection And Their Dysregulation In X-linked Lymphoproliferative Disease
Funder
National Health and Medical Research Council
Funding Amount
$453,986.00
Summary
EBV is ubiquitous virus that infects more than 90% of the population worldwide. Although infection is largely asymptomatic in most healthy individuals, EBV is nonetheless associated with the development of at least 7 distinct types of human malignancies. Most importantly, EBV is still a huge healthy problem in conditions of immune suppression. Therefore a better understanding of the mechanisms involved in effective control of the virus will help develop better immune therapies and vaccines.
CD8+ T cells provide us with protection against viruses and can also mediate potent anti-tumour effects. Understanding the signals that initiate and sustain an effective CD8+ T cell response is important if we are to intervene in diseases where CD8+ T cell function is defective. We will study patients with inherited gene defects that disrupt some of the signals that T cells receive to determine the role those signals usually play in instructing CD8+ T cells to fight viral infection.
This fellowship is to support Professor Stephen Kent in generating new advances in vaccines to prevent HIV (the cause of AIDS) and Influenza (“The Flu”). HIV causes over 1.5 million deaths per year and no vaccine is currently available. Influenza causes around half a million deaths per year. Although the current Influenza vaccine is partially effective, improvements are needed for it to be able to protect against the many different strains of Influenza that can cause infection.
Using A Novel Assay That Detects Antigen Specific CD4+ And Regulatory T Cells To Further Understand Reconstitution Of Antigen Specific Immune Response Post Anti-retroviral Therapy In Subjects With HIV And In The Diagnosis Of Latent TB
Funder
National Health and Medical Research Council
Funding Amount
$102,780.00
Summary
The process by which the immune system recovers after commencement of therapy for HIV is not well understood. We will use a new test to monitor the immune system's ability to recognise and react to different antigens inorder to understand the factors that affect immune recovery in patients on therapy for HIV. We will also evaluate the use of this new test in the diagnosis of latent TB. Improvement in detection will lead to treatment of latent TB thus reduction of cases of active TB.