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PhD Exit Seminar – Kewei Xu (Harrison lab)

September 29, 2016 @ 10:10 am - 11:10 am

PhD Exit Seminar


Thursday September 29th, 10:10 am – Room SW 403, University of Toronto at Scarborough


Kewei Xu (Harrison lab)

Cytoskeletal changes during classical activation of macrophages


As effector cells of the innate immune response, macrophages are capable of recognizing and eliminating pathogens during inflammation. Macrophages achieve maximal immunological potential by undergoing cellular activation. Classical activation of macrophages (M1) with interferon-γ (IFNγ) and lipopolysaccharide (LPS) greatly enhances the immune response against intruding pathogens. We have previously revealed that stathmin association with microtubules (MTs) is considerably reduced in M1 macrophages using proteomics approaches. In this thesis, we demonstrate a LPS-dependent stathmin protein reduction in M1 macrophages. We also explored the functional roles of stathmin down-regulation by generating stable cell lines overexpressing stathmin-GFP. Stathmin-GFP overexpression impaired MT integrity and reduced activation-associated phenotypes. Furthermore, overexpressing stathmin-GFP inhibited complement receptor 3 (CR3)-mediated phagocytosis and cellular activation, implicating its pivotal inhibitory role in classical activation of macrophages.



September 29, 2016
10:10 am - 11:10 am
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