Research Interests:
My lab is interested in how a healthy immune system balances being ready to react by swiftly fighting off pathogens, while maintaining tolerance to harmless challenges such as food and body tissues. My lab is focused on the molecular basis of function and fitness in human regulatory T cells, and the role of the transcription factor FOXP3 in orchestrating this. There is increasing evidence that in a wide number of disease states including autoimmune diseases such as Type 1 diabetes and IBD, Treg cells fail to regulate the immune system effectively, and allow inappropriate destruction of tissues that are essential for life. In order to understand how this breaks down in disease one must first understand what is the basis of a healthy Treg. To do this we use a number of state of the art gene discovery tools such as microarrays and next generation sequencing to identify and then confirm the key genes in Treg function. We were the first to identify the targets of FOXP3 in human Treg using chromatin immunoprecipitation, and we are now developing systems biology approaches to modeling the gene regulation networks in human Treg from healthy and disease samples. Tight regulation of target genes including SATB1 by FOXP3 and microRNAs is a key mechanism by which Treg retain their phenotype, and breakdown of this results in loss of function. Most recently we have established chromatin conformation capture in order to fully map the regulatory interactions inhuman Treg. A key goal of our research is to fully map the defects resulting in loss of Treg function in disease, so that new approaches to preventing or reversing this can be developed.
Training:
After a B.Sc (hons) at Kings College London and Ph.D at Mill Hill, London, Dr Barry undertook postdoctoral training in Adelaide and at the University of Washington in Seattle. He then spent 4 years working as a discovery scientist at Immunex and AMGEN in the US, prior to returning to Adelaide to set up a lab.