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This study will investigate the why disease is worse in infants and how early life viral infection impacts the developing immune system.
This is a strategic “pilot” project in which we are seeking basic information on the immune cell content of gestational tissues.
This project investigates how different populations of cells within the respiratory tract immune system are altered during a viral infection.
Allergic sensitization and reduced ability to respond to viral infections may contribute to virus-induced wheeze and asthma development in young children. Plasmacytoid dendritic cells (pDC) are rare immune cells that produce type I interferons (IFN-I) and play a key role in orchestrating immune responses against viruses.
Impaired interferon response and allergic sensitization may contribute to virus-induced wheeze and asthma development in young children. Plasmacytoid dendritic cells play a key role in antiviral immunity as critical producers of type I interferons.
IgE-mediated sensitisation to egg is common in infants. In some cases, the processes leading to egg sensitisation are established in early life, even before introduction to solid foods. The underlying mechanisms remain poorly understood.
Food allergy affects up to 10% of Australian infants. It was hypothesized that if parents follow the Australasian Society of Clinical Immunology and Allergy guidelines, Australian food allergy rates may stabilize or decline.
The aim of this review was to map the literature assessing associations between maternal or infant immune or gut microbiome biomarkers and child neurodevelopmental outcomes within the first 5 years of life. We conducted a PRISMA-ScR compliant review of peer-reviewed, English-language journal articles.
Malaria is a deadly disease caused by Plasmodium spp. Several blood phenotypes have been associated with malarial resistance, which suggests a genetic component to immune protection.
Tissue-resident memory T (TRM) cells have emerged as key players in the immune control of melanoma. These specialized cells are identified by expression of tissue retention markers such as CD69, CD103 and CD49a with downregulation of egress molecules such as Sphingosine-1-Phosphate Receptor-1 (S1PR1) and the lymphoid homing receptor, CD62L.