My lab is focused on understanding the development and function of the immune system. Our studies are set in the contexts of in vivo models of pathogenesis and health so as to set the stage for translation into humans of new diagnostics and therapeutics. Current projects explore models of infectious, allergic, autoimmune and neoplastic disease from the perspective of a new signalling pathway involving an epigentic regulatory protein called Mina. This protein belongs to the large and evolutionarily conserved Jumonji C family of dioxygenases, many of whose members are involved in epigenetic gene regulation. To date, important roles for Mina have been discovered in both CD4 T cells and intestinal epithelial cells (IECs).
T helper 17 (Th17) cells are a sub-type of CD4 T cells known to be important in protection from extracellular bacterial and fungal pathogens. Disregulation of their development or function can lead to susceptibility to infectious, allergic and autoimmune diseases. We have discovered that proper development of Th17 cells requires Mina; and that Mina's absence attenuates paralytic disease in a Th17-dependent model of multiple sclerosis. Currently, we are exploring: (1) the detailed molecular mechanism by which Mina exerts its influence on Th17 cell development; and (2) the physiological scope of Mina's Th17-dependent role in infectious, autoimmune and allergic disease. In particular, we are interested in understanding whether Mina's in vivo role extends to the development and maintenance of Th17 memory and pathogenicity.
Alpha-defensins (or, in mouse, cryptdins) are a family of cationic anti-microbial peptides secreted by paneth cells located at the base of Crypts of Lieberkhun found in the small intestine. They are critical in providing a first line of defense against microbial pathogens. They are also important in shaping commensal microbiota diversity, recently found to play vital roles in multiple physiological processes, including digestion and immune system development. We have recently discovered that during mucosal inflammation of the gut, Mina plays a critical role in repressing the expression of alpha-defensins. In Mina's absence, alpha-defensin expression is de-repressed and the capacity to expel parasitic helminths and susceptibility to intestinal adenomagenesis are both enhanced. Current studies are focused on exploring whether alpha-defensins are causally linked to helminth infection and intestinal cancer.
Associate Professor: Dr. Mark Bix
Assistant Professor: Dr. Belgacem Mihi
research technical associate
masters course student
Ph.D. course student
Co-inventor of International Patent Application titled "Mice Having beta 2 Microglobulin Gene Disruption" published June 11, 1992 as Pub. No. WO 09/0209688.
Inventor of Tangible research property described in The Journal of Immunology, 1998, 161:3271-3281 titled “NK T Cell Hybridoma, DN3A4-1.2”.
Co-inventor of United States Patent Application titled “Methods and Compositions for Predicting Development of Atopic Diseases” published November 3, 2011 as Pub. No. US 2011/0269125 A1
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