Troy Baldwin
University of Alberta, AB

Troy Baldwin completed his Ph.D. training in Dr. Hanne Ostergaard’s laboratory at the University of Alberta where he was interested in understanding the role of the extracellular domain of the protein tyrosine phosphatase CD45. In 2002, he started his post-doctoral fellowship with Dr. Kristin Hogquist in the Center for Immunology at the University of Minnesota. It was here where his interest in T cell development began. In 2007, Dr. Baldwin started his own independent laboratory in the Department of Medical Microbiology and Immunology at the University of Alberta. His current research is aimed at determining how signals received by an immature thymocyte promote either survival and differentiation (positive selection and lineage commitment) or cell death (negative selection). He utilizes in vivo mouse models to address the molecular mechanisms underlying this binary fate decision in hopes of one day understanding how the immune system naturally induces self-tolerance.

Javier M Di Noia
Institut de Recherches Cliniques de Montréal (IRCM), PQ

Dr Javier M Di Noia graduated in Biological Sciences from the University of Buenos Aires, Argentina. As a PhD student he characterized the genetic diversity and role of a family of surface molecules from the human pathogen Trypanosoma cruzi, under the supervision of Dr Alberto C.C. Frasch. After obtaining his PhD in 2000, Dr Di Noia moved to the MRC-Laboratory of Molecular Biology in Cambridge, UK for post-doctoral training with Dr Michael S. Neuberger. There he continued to worked on the mechanisms generating antibody diversity by somatic hypermutation and class switch recombination. He took a position as director of a research unit at the Institut de Recherches Cliniques de Montréal (IRCM) in June 2006 where he continues to be interested in antibody diversification as a paradigmatic example of genetic diversity generation. The focus of his laboratory is on the mechanisms of antibody diversification in mature B cells. These mechanisms allow an efficient humoral immune response during infection by increasing the size and affinity of the antibody repertoire, isotype switching and generating the B-cell memory underpinning the efficacy of vaccination. However, as antibody diversification entails DNA damage in the B cell genome, it must minimize the chances of oncogenic side effects such as widespread mutation and chromosomal translocations. The laboratory is working on understanding the initiation; regulation and processing of the DNA damage actively introduced by the enzyme Activation Induced Deaminase in the immunoglobulin genes of activated B cells. They have recently identified mechanisms determining the subcellular localization of Activation Induced Deaminase so as to regulate its access to the genome. The laboratory is also exploring other systems that may produce genetic diversity through active mutagenesis and could be at work in human pathogens. Dr Di Noia holds a Canada Research Chair in Genetic Diversity. He has appointments as Assistant Research Professor with the Department of Medicine at the University of Montréal and as Adjunct Professor with the Department of Medicine at McGill University.