Prof Robert Brink
Senior Principal Research Fellow
Robert 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.
In the NewsA trigger that likely unleashes autoimmune disease - May 13, 2015
How the immune system positions its gatekeepers - Mar 18, 2013
How infection can trigger autoimmune disease - Nov 09, 2012
Creating clarity around a key aspect of the immune system - Aug 16, 2010
Mystery solved at crossroads of immune response - Jul 17, 2009
B cell mutations that may cause cancers and autoimmune diseases - Feb 29, 2008
Awards and Honours
2011 - NHMRC Senior Research Fellowship, Level B
2011 - Conjoint Associate Professor, University of New South Wales
2006 - NHMRC Senior Research Fellowship, Level A
1987 - BSc (Hons), University of Sydney - Australia
Tangye SG, Brink R, Goodnow CC, Phan TG. 2015. Snapshot: Interactions between B cells and T cells. Cell (in press 13 August 2015) 162:926
Butt D, Chan TD, Bourne K, Hermes JR, Nguyen A, Stratham A, O’Reilly L, Strasser A, Price S, Schofield P, Christ D, Basten A, Ma C, Tangye S, Phan TG, Rao VK and Brink R. FAS inactivation releases "Rogue" Germinal Center B cells that escape antigen control and drive IgE and autoantibody production. Immunity. May 2015; 890-902.
Brink R, Paus D, Bourne K, J.R. Hermes, Gardam S, Phan T.G, Chan T.D The SWHEL system for high-resolution analysis of in vivo antigen-specific T-dependent B cell responses. April 2015. Methods Mol Biol; 1291;103-123
Gatto D, Wood K, Caminschi I, Murphy-Durland D, Schofield P, Christ D, Karupiah G and Brink R. (2013) The chemotactic receptor EBI2 regulates the homeostasis, localization and immunological function of splenic dendritic cells. Nature Immunol. 14: 446-453.
ChanTD, WoodK, Hermes JR, ButtD, JollyCJ, BastenA and Brink R. (2012) Elimination of germinal-center-derived self-reactive B cells is governed by the location and concentration of self-antigen. Immunity 37: 893-904.
Gardam S*, Turner VM*, Anderton H, Limaye S, Basten A, Koentgen F, Vaux DL, Silke J** and Brink R**. (2011) Deletion of cIAP1 and cIAP2 in murine B lymphocytes constitutively activates cell survival pathways and inactivates the germinal center response. Blood 117: 4041-4051. *SG and VMT contributed equally, ** JS and RB contributed equally
Goodnow CC, Vinuesa CG, Randall K, Mackay F and Brink R. (2010) Control systems and decision-making for antibody production. Nat. Immunol. 11: 681-688.
Gatto D, Paus D, Basten A, Mackay C and Brink R. (2009) Guidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses. Immunity. 31: 259-269.
Chan TD, Gatto D, Wood K, Camidge T, Basten A and Brink R. (2009) Antigen affinity controls rapid T-dependent antibody production by driving the expansion rather than the differentiation or extrafollicular migration of early plasmablasts. J. Immunol. 183: 3139-3149.
Gardam S, Sierro F, Basten A, Mackay F and Brink R. (2008) TRAF2 and TRAF3 signal adapters act cooperatively to control the maturation and survival signals delivered to B cells by the BAFF receptor. Immunity. 28: 391-401.
Phan TG, Paus D, Chan TD, Turner ML, Nutt SL, Basten A and Brink R. (2006). High affinity germinal center B cells are actively selected into the plasma cell compartment. J. Exp. Med. 203: 2419-2424.
Paus D, Phan TG, Chan TD, Gardam, S, Basten A and Brink R. (2006) Antigen recognition strength regulates the choice between extrafollicular plasma cell and germinal center B cell differentiation. J. Exp. Med. 203: 1081-1091.
Grech AP, Gardam S, Chan T, Quinn R, Gonzales R, Basten A and Brink R. (2005) Tumor necrosis factor receptor 2 (TNFR2) signaling is negatively regulated by a novel, carboxyl-terminal TNFR associated factor 2 (TRAF2) binding site. J. Biol. Chem. 280: 31572-31581.
Grech AP, Amesbury M, Chan T, Gardam S, Basten A and Brink R. (2004) TRAF2 differentially regulates the canonical and non-canonical pathways of NF-kB activation in mature B cells. Immunity. 21: 629-642.
Thien M, Phan TG, Gardam S, Amesbury M, Basten A, Mackay F and Brink R. (2004) Excess BAFF rescues self-reactive B cells from peripheral deletion and allows them to enter forbidden follicular and marginal zone niches. Immunity. 20: 785-798.
Phan TG, Amesbury M, Gardam S, Crosbie J, Hasbold J, Hodgkin PD, Basten A and Brink R. (2003) B cell receptor-independent stimuli trigger immunoglobulin (Ig) class switch recombination and production of IgG autoantibodies by anergic self-reactive B cells. J. Exp. Med. 197: 845-860.
Brink R and Lodish HFL. (1998) Tumor necrosis factor receptor (TNFR)-associated factor 2A (TRAF2A), a TRAF2 splice variant with an extended RING finger domain that inhibits TNFR2-mediated NF-kB activation. J. Biol. Chem. 273: 4129-4134.
Brink R, Goodnow CC, Crosbie J, Adams E, Eris J, Mason DY, Hartley SB and Basten A. (1992) Immunoglobulin M and D antigen receptors are both capable of mediating B lymphocyte activation, deletion, or anergy after interaction with specific antigen. J. Exp. Med. 176: 991-1005.