Head of laboratory
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Research conducted by this unit focuses on mucosal immunity, at both a molecular and cellular level. More specifically, this unit investigates the involvement of a number of genes (traditionally associated with the control of the immune response) in experimental models of idiopathic inflammatory bowel disease and atherosclerosis, with a view to gaining new insights into the mechanisms which underlie these disorders.
Cytokine regulation of intestinal mucosal immunity. The development of two lineages of murine B cells (B1 and B2 cells) in the intestinal mucosa are being investigated, using cytokine gene knock out mice. Although we found that conventional B2 cells are dependent on IL-6, whereas B1 cells rely on IL-5, the precise mechanism(s) underlying these interactions still remains to be explored. More recently, we have been using STAT3 signal transduction gene knock-in mice, and IL-5Rbgene knockout mice, to explore whether these two signal transduction pathways are critical for B2 or B1 cell maturation, respectively.
The pathogenesis of atherosclerosis. Using a microvascular surgical technique, we have successful developed a unique mouse model of endothelial damage/neointimal proliferation that has allowed us to access gene knockout mice to selectively examine the effects of specific proteins in neointimal proliferation.