David Gray



1980-1983    PhD in Immunology; Dept. of Immunology, University of Birmingham

1983-1985    Postdoc; Dept. of Immunology, University of Birmingham

1985-1991    Scientific Member, Basel Institute for Immunology, Basel, Switzerland

1991-1998    Wellcome Trust Senior Research Fellow and Honorary Reader/Professor of Cellular Immunology, Royal Postgraduate Medical School, Hammersmith Hospital, London

1998-2002    Wellcome Trust Senior Research Fellow and University Professorial Fellow, ICAPB, University of Edinburgh

2002-Present    Professor of Immunology, IIIR, University of Edinburgh

Research summary

Innate responses of B cells: As part of the adaptive immune system, B cells generally see their environment via recognition of antigens with their BCR. However, like other antigen presenting cells, they also express pattern recognition receptors (eg. Toll-like receptors, TLRs) normally associated with cells of the innate immune system. Their responses to stimulation via these receptors are many and varied (eg. proliferation, antibody production, cytokine secretion and enhanced antigen presentation). We are currently investigating the effects of TLR ligation on B cell subsets and the influence that this has on the development of T cell responses. We are using a model infection ( Salmonella), in which the pathogen can deliver a variety of TLR ligands to activate B cells in BCR-independent fashion.

Immune regulation by B cells: As well as antibodies, B cells make cytokines, following activation via BCR or CD40 or after ligation of TLRs. IL-10 is one of the most abundant cytokines made by B cells (in particular, by marginal zone B cells). We know that this B cell-derived IL-10 is necessary for resolution of autoimmune inflammation in several disease models. We are currently investigating the mechanism of this regulation, for instance, by programming development of regulatory T cells.

Immunological memory: Memory is a defining feature of the immune system. In "remembering" previous encounters with infectious organisms it reacts more rapidly and more efficiently (e.g. higher affinity) and so, is the basis for vaccination against disease. The basis of this memory to a large extent is the maintenance of increased frequency of antigen-specific memory cells. Memory B cells, CD4 T cells and CD8 T cells exhibit differences in the way that they are maintained over long periods. We are currently interested in the long-term survival of memory CD4 + T cells and the role of B cells as antigen presenting cells in this process.

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