Dr Pablo Silveira
Senior Research Officer; Group Leader, Autoimmunity Research Unit, Garvan Institute of Medical Research; Conjoint Senior Lecturer Faculty of Medicine, The University of New South Wales
Email: p.silveira"at"garvan.org.au
Research Group: B Cell Tolerance
Pablo has also contributed to work that has demonstrated the important role of B lymphocytes in the development of type 1 diabetes. His current work focuses on genetic, molecular and cellular defects that give rise to B cells with a capacity to contribute to autoimmune diseases such as type 1 diabetes and lupus.
Education
2000 PhD, University of Sydney
1996 B Med Sci (Hons 1), University of Sydney
Awards and Honours
2003 Clive and Vera Ramaciotti Establisment Grant ($30 000)
2003 Cecelia Kilkeary Small Equipment Grant
2003 Peter Doherty (NHMRC) Postdoctoral Fellowship
2001 Juvenile Diabetes Foundation Postdoctoral Fellowship
1999 AMRAD Travel Scholarship
1997 Australian Society of Immunology Student Travel Prize
1997 Australian Postgraduate Award
1995 Juvenile Diabetes Foundation Australia Summer Student Scholarship
Publications
Silveira PA, Grey ST. B cells in the spotlight: innocent bystanders or major players in the pathogenesis of type 1 diabetes. Trends Endocrinol Metab 2006; 17(4):128-35.
Chen YG, Silveira PA, Osborne MA, Chapman HD, Serreze DV. Cellular expression requirements for inhibition of type 1 diabetes by a dominantly protective major histocompatibility complex haplotype. Diabetes 2007; 56(2):424-30.
Silveira PA, Chapman HD, Stolp J, Johnson E, Cox SL, Hunter K, Wicker LS, Serreze DV. Genes within the Idd5 and Idd9/11 Diabetes Susceptibility Loci Affect the Pathogenic Activity of B Cells in Nonobese Diabetic Mice. J Immunol 2006; 177(10):7033-41.
Silveira PA, Dombrowsky J, Johnson E, Chapman HD, Nemazee D, Serreze DV. B cell selection defects underlie the development of diabetogenic APCs in nonobese diabetic mice. J Immunol 2004; 172(8):5086-94.
Silveira PA, Johnson E, Chapman HD, Bui T, Tisch RM, Serreze DV. The preferential ability of B lymphocytes to act as diabetogenic APC in NOD mice depends on expression of self-antigen-specific immunoglobulin receptors. Eur J Immunol 2002; 32(12):3657-66.
Johnson EA, Silveira P, Chapman HD, Leiter EH, Serreze DV. Inhibition of Autoimmune Diabetes in Nonobese Diabetic Mice by Transgenic Restoration of H2-E MHC Class II Expression: Additive, but Unequal, Involvement of Multiple APC Subtypes. J Immunology 2001; 167:2404-2410
Silveira PA, Wilson WE, Esteban LM, Jordan MA, Hawke CG, van Driel IR, Baxter AG. Identification of the Gasa3 and Gasa4 autoimmune gastritis susceptibility genes using congenic mice and partitioned, segregative and interaction analyses. Immunogenetics 2001; 53(9):741-50.
Jordan MA, Silveira PA, Shepherd DP, Chu C, Kinder SJ, Chen J, Palmisano LJ, Poulton LD, Baxter AG. Linkage analysis of systemic lupus erythematosus induced in diabetes-prone nonobese diabetic mice by Mycobacterium bovis. J Immunol 2000; 165(3):1673-84.
Silveira PA, Baxter AG, Cain WE, van Driel IR. A major linkage region on distal chromosome 4 confers susceptibility to mouse autoimmune gastritis. J Immunol 1999; 162(9):5106-11.
Hammond KJ, Poulton LD, Palmisano LJ, Silveira PA, Godfrey DI, Baxter AG. alpha/beta-T cell receptor (TCR)+CD4-CD8- (NKT) thymocytes prevent insulin-dependent diabetes mellitus in nonobese diabetic (NOD)/Lt mice by the influence of interleukin (IL)-4 and/or IL-10. J Exp Med 1998; 187(7):1047-56.
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