Professor Robert Brink
Professor Robert Brink obtained his Honours degree in Science from the University of Sydney in 1987 where he majored in Biochemistry and Genetics. He completed his PhD in 1992 under the supervision of Antony Basten and Chris Goodnow at Sydney’s Centenary Institute, where he worked on novel transgenic mouse models of B cell self-tolerance. In 1994 he took up a postdoctoral position in the laboratory of Harvey Lodish at the Whitehead Institute in Boston, where he investigated how the newly identified TRAF family of intracellular proteins function in signal transduction by cell membrane receptors. Upon returning to the Centenary Institute in 1996, Robert developed a number of genetically modified mouse models designed to elucidate in vivo B cell responses and TRAF protein function. These models have been successfully employed within his laboratory and in laboratories around the world to make landmark findings published in journals such as Immunity, J. Exp. Med., Cell and Nature Immunology. In 2006 Robert was recruited to the Garvan Institute of Medical Research in Sydney to head the B Cell Biology laboratory. In 2010, he was appointed Head of the Institute’s Immunology Research Division. He was appointed Conjoint Associate Professor at the University of NSW in 2011 and Conjoint Professor in the Faculty of Medicine 2014. Robert is a Senior Research Fellow of the National Health and Medical Research Council (NHMRC) and member of an NHMRC Program Grant team since 2002. His major research focus is the regulation B cell survival and antibody production during protective immune responses and how these processes contribute to diseases such as autoimmunity, allergy and cancer.
β-cell function is regulated by metabolic and epigenetic programming of islet-associated macrophages, involving Axl, Mertk, and TGFβ receptor signaling.
- 2023The Journal of experimental medicine10.1084/jem.20221020
Human PIK3R1 mutations disrupt lymphocyte differentiation to cause activated PI3Kδ syndrome 2.
- 2023Frontiers in immunology10.3389/fimmu.2023.1095257
gain-of-function mutation drives cell-autonomous accumulation of PD-1 ICOS activated T cells, T-follicular, T-regulatory and T-follicular regulatory cells.
Apoptotic cell fragments locally activate tingible body macrophages in the germinal center.
Skin γδ T cell inflammatory responses are hardwired in the thymus by oxysterol sensing via GPR183 and calibrated by dietary cholesterol.