The Type I Interferon Anti-Viral Pathway Contributes To Macrophage Polarization Following Infection With Oncolytic Vesicular Stomatitis Virus
- ASU Author/Contributor (non-ASU co-authors, if there are any, appear on document)
- Sylas Owen (Creator)
- Institution
- Appalachian State University (ASU )
- Web Site: https://library.appstate.edu/
- Advisor
- Maryam Ahmed
Abstract: Vesicular stomatitis virus (VSV) is a promising oncolytic agent that directly kills cancer cells, but which also modulates immune elements within the tumor microenvironment. Here we were interested in how VSV affects tumor-associated macrophages (TAMs), a cell type that interconverts along a spectrum of polarizations from pro-cancer M2 to anti-cancer M1 subtypes. We hypothesized that VSV infections would switch M2 TAMs to an M1 phenotype via activation of the type I interferon anti-viral response. Such was the case with a mutant strain of VSV (rM51R-M) where the lack of a functional M protein led to activation of the anti-viral response and the upregulation of M1 markers (i.e. IFNa, STAT1, P-STAT1, MHC-II, and CD80, but not IRF5) in model M2 THP-1 macrophages. Our data suggest that rM51R-M virus has a previously unappreciated immunogenic potential based on modulation of TAM phenotypes.
The Type I Interferon Anti-Viral Pathway Contributes To Macrophage Polarization Following Infection With Oncolytic Vesicular Stomatitis Virus
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Created on 10/12/2020
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Additional Information
- Publication
- Thesis
- Owen, S. (2020). The Type I Interferon Anti-Viral Pathway Contributes To Macrophage Polarization Following Infection With Oncolytic Vesicular Stomatitis Virus. Unpublished Master’s Thesis. Appalachian State University, Boone, NC.
- Language: English
- Date: 2020
- Keywords
- Oncolytic virotherapy,
Tumor-associated macrophage,
Vesicular stomatitis virus,
Type I Interferon,
rM51R-M virus