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dc.contributorFink, Rachel
dc.contributorDouglas, Amber
dc.contributor.advisorStranford, Sharon
dc.contributor.authorZimmermann, Barret
dc.description.abstractMurine AIDS is an animal model used to study human AIDS. Infection of susceptible strains of mice such as C57BL/6 with murine leukemia virus (MuLV) leads to MAIDS in a manner analogous to HIV-induced AIDS. Conversely, MAIDS resistant strains like BALB/c generate a successful immune defense against the virus after infection. Dendritic cells (DCs) play the largest role in viral particle processing and activation of naïve T cells, which elicit immune responses that can eradicate HIV or MuLV infection. The few published studies that have examined the role of a specific DC subset, plasmacytoid dendritic cells (pDCs), in AIDS, express opposing views; some argue that pDCs inhibit HIV spread, while others argue pDCs promote it. We used flow cytometry to compare pDC percentages in the spleens of BALB/c and C57BL/6 mice one week post-infection. Firstly, we identified a larger pDC (CD317+ and CD45R+) population in the susceptible strain after infection; this difference was statistically significant (p <.0001). These findings suggested that pDCs may be associated with disease vulnerability. Secondly, phenotypic differences were observed between strains, suggesting that these cell populations may be distinct. Nevertheless, the observed strain-specific differences in CD317+CD45+ population might influence disease susceptibility in MAIDS, and correspondingly could influence our understanding of human AIDS-susceptibility.en_US
dc.description.sponsorshipBiological Sciencesen_US
dc.rightsAttribution 3.0 Unported
dc.subjectplasmacytoid dendritic cellsen_US
dc.subjectflow cytometryen_US
dc.subjectmurine acquired immunodeficiency syndromeen_US
dc.titleThe Role of Plasmacytoid Dendritic Cells (pDCs) in Murine Acquired Immunodeficiency Syndrome (MAIDS)en_US
mhc.institutionMount Holyoke College

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Attribution 3.0 Unported
Except where otherwise noted, this item's license is described as Attribution 3.0 Unported