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PhD Exit Seminar
Kewei Xu
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.
Thursday, September 29th, 2016 at 10:10 am
SW 403 – University of Toronto at Scarborough
Supervisor: Prof. Rene Harrison
[email protected]
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