Dr Robert Brink
Senior Research Fellow; Group leader, B Cell Immunobiology, Autoimmunity Research Unit, Garvan Institute of Medical Research
Email: r.brink 'at' garvan.org.au
Research Group: B Cell Immunobiology
Robert undertook his postdoctoral studies at the Whitehead Institute in Boston, where he furthered his molecular skills and worked on TNF receptors their signalling molecules. Upon returning to Australia, he generated gene-targeted mice designed with which to visualise B cell responses and analyse gene function in vivo. Robert joined Garvan as a Senior Research Fellow in 2006 and continues to use these in vivo models to uncover how B cells function during protective immune responses, autoimmune disease and lymphomagenesis.
Publications
Brink R. Germinal-center B cells in the zone. Immunity 2007; 26:552-4.
Phan TG, Paus D, Chan TD, Turner ML, Nutt SL, Basten A, Brink R. High affinity germinal center B cells are actively selected into the plasma cell compartment. Journal of Experimental Medicine 2006; 203:2419-24.
Paus D, Phan TG, Chan TD, Gardam S, Basten A, Brink R. Antigen recognition strength regulates the choice between extrafollicular plasma cell and germinal center B cell diff erentiation. Journal of Experimental Medicine 2006; 203:1081-1091.
Grech AP, Gardam S, Chan T, Quinn R, Gonzales R, Basten A, Brink R. Tumor necrosis factor receptor 2 (TNFR2) signaling is negatively regulated by a novel, carboxyl-terminal TNFR-associated factor 2 (TRAF2)-binding site. Journal of Biological Chemistry 2005; 280:31572–81
Grech AP, Amesbury M, Chan T, Gardam S, Basten A, Brink R. TRAF2 differentially regulates the canonical and noncanonical pathways of NF-κB activation in mature B cells. Immunity 2004; 21:629-42
Thien M, Phan TG, Gardam S, Amesbury M, Basten A, Mackay F, Brink R. Excess BAFF rescues self-reactive B cells from peripheral deletion and allows them to enter forbidden follicular and marginal zone niches. Immunity 2004; 20:785-98
Phan TG, Amesbury M, Gardam S, Crosbie J, Hasbold J, Hodgkin PD, Basten A, Brink R. B cell receptor-independent stimuli trigger immunoglobulin (Ig) class switch recombination and production of IgG autoantibodies by anergic self-reactive B cells. Journal of Experimental Medicine 2003; 197:845-60
Brink R, Lodish HFL. Tumor necrosis factor receptor (TNFR)-associated factor 2A (TRAF2A), a TRAF2 splice variant with an extended RING finger domain that inhibits TNFR2-mediated NF-κB activation. Journal Biological Chemistry 1998; 273:4129-34.
Brink R, Goodnow CC, Crosbie J, Adams E, Eris J, Mason DY, Hartley SB, Basten A. Immunoglobulin M and D antigen receptors are both capable of mediating B lymphocyte activation, deletion, or anergy after interaction with specific antigen. Journal of Experimental Medicine 1992; 176:991-1005.
Goodnow CC, Brink R, Adams E. Breakdown of self-tolerance in anergic B lymphocytes. Nature 1991; 352:532-6.
