Research Interest: In multiple sclerosis and its murine model, experimental autoimmune encephalitis (EAE), increase in vascular permeability leads to extravasation of fibrinogen, which is deposited in the intercellular space. Fibrinogen is a substrate for cell adhesion mediated by CD11b, an integrin-like molecule expressed on the surface of both CNS-resident (microglia) and blood-borne (monocytes) innate immune cells. Blockage of fibrinogen-CD11b interactions by administration of competitor peptides has led to amelioration of EAE disease, and this finding has been interpreted as evidence of a role for this interaction in the activation of microglia. However, our past work (Ajami et al Nature Neuroscience 2011) indicated that microglia play a limited role in disease progression, while monocytes are critical. Using parabiosis-irradiation-separation models unique to our laboratory, I am part of a team that investigates an alternative interpretation of the role of fibrinogen-CD11b interactions. This model allows for the replacement of circulating, but not CNS resident innate immune cells, with transgenically labelled donor cells, and thus for the dynamic assessment of monocyte infiltration in the CNS and their fate during EAE. Specifically, we investigate wether blocking fibrinogen-CD11b interactions will specifically reduce monocytic infiltration rather than microglial activation.
I am currently an undergraduate student at Queen’s University studying Biochemistry and Life Sciences. Outside of the lab, I love to spend time with family and friends and enjoy breakdancing, basketball, soccer, and producing hip hop music! I am also keen on global health initiatives and community medicine. I joined the Rossi Lab in the summer of 2011 as a high school senior, having awesome mentors such as Dr. Bahareh Ajami and Dr. Leslie So Alfaro. and again in the summer of 2013 as a Centre for Blood Research Undergraduate fellow under the guidance of Dr. Coral Ann Lewis in the Dr Rossi’s Lab!