Name Christopher Rudd | ||
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Christopher Edward Rudd is a Canadian-born immunologist-biochemist. He is currently Professor of Molecular Immunolology at the University of Cambridge, as well as the Head of the Cell Signalling Section. [2]
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Early life and education
Chris Rudd was born in Toronto, Canada. He was educated at the Jesuit-run Brebeuf College School and at McGill University in Montreal and received an MSc degree from the Universite d'Ottawa and PhD and DSc degrees from University College, London. He held faculty positions at Harvard Medical School and Imperial College London before moving to Cambridge University.
Research
Rudd is credited with having had a major impact on the understanding of the intracellular signals that control T-cell immunity. Rudd was the first to discover that intracellular protein kinases interact with surface receptors, by identifying the interaction of T-cell co-receptors CD4 (also the receptor for the human immunodeficiency virus, HIV-1) and CD8 on T-cells with protein-tyrosine kinase p56lck. His discovery provided a role for members of the proto-oncogene pp60src kinase family in normal cell signaling. Other receptors were later found to use src-related kinases to regulate cell growth. In terms of immunology, the CD4- and CD8-p56lck complexes are now widely accepted as the initiators of the T cell activation, leading to the recruitment of a second tyrosine kinase ZAP-70 that control the ability of T-cells to respond to foreign pathogens, allogeneic transplants and cancer cells.
In a second area, Rudd elucidated signaling mechanisms by which co-receptors CD28 and CTLA-4 modulate T-cell responses. By showing that CTLA-4 activates T-cell motility and migration, he has proposed the 'reverse-stop signal model' to account for CTLA-4 down regulation of the responses of conventional T-cells to antigen. His research has also shown that a mutant form of an adapter protein termed ADAP can block the infection of T-cells by the Human Immunodeficiency Virus (HIV-1) by simultaneously interfering with HIV-1 replication and the transmission of the virus between T-cells. Rudd's work has had important clinical outcomes as it laid the foundation for Chimeric antigen receptor (CAR) cancer therapy that has been pioneered by Carl June at the University of Pennsylvania. T cells transduced with chimeric receptors to recognize and kill cancer cells have employed immunoreceptor tyrosine-based activation motifs (ITAMs) (a target of p56lck), as well as CD28 signaling motifs that were identified by Rudd's lab.
Recognition
Rudd has received awards including the Cancer Research Institute/Benjamin Jacobson Family Investigator Award (New York), Claudia Adams Barr Research Award (Boston) and was a Scholar of the Leukemia Society of America and a Principal Research Fellow (PRF) of the Wellcome Trust. He was elected a Fellow of the Royal College of Pathologists (FRCPath) and the Academy of Medical Sciences (FMedSci). Over the years Rudd has trained many graduate students at Ph.D. level, some of whom hold prestigious academic positions in different parts of the world.
His nomination as a Fellow of the Academy of Medical Sciences (FMedSci) in 2002 reads,
"He has made major contributions to our understanding of T cell activation, and has defined several of the key molecular pathways that connect cell membrane receptor ligation with gene transcription. In particular he made the seminal discovery that that CD4 and CD8 co-receptor molecules are linked to the p56 lck src family kinase. These complexes are now widely accepted as the initiators of T cell activation of phosphorylation of several key substrates. These observations have had important implications in the field of oncology, since for the first time, a function was provided for the p60 src family of proto-oncogenes in normal cell growth."
http://www.acmedsci.ac.uk/fellows/fellows-directory/ordinary-fellows/professor-christopher-rudd/