Show simple item record

dc.contributor.author Liu, Li en_US
dc.date.accessioned 2007-07-12T17:50:11Z
dc.date.available 2007-07-12T17:50:11Z
dc.date.issued 2001-04-01T00:00:00Z en_US
dc.identifier.uri http://hdl.handle.net/1993/2593
dc.description.abstract Chlamydia, an obligate intracellular bacterial pathogen, can successfully infect a wide range of host species and persist in the infected hosts for a long period of time, suggesting that 'Chlamydia' may have evolved strategies for escaping host defense mechanisms. We have found that ' Chlamydia' indeed possesses the ability to evade host immune recognition. Immune recognition is a requirement for hosts to develop an effective immunity against microbial infections. It has been shown that MHC class II-mediated immune responses often play a critical role in controlling intracellular pathogen infection. We hypothesized that 'Chlamydia' may suppress MHC class II expression in order to escape MHC class II-mediated immune responses. We compared the IFN-_-inducible MHC class II expression between epithelial cells with or without chlamydial infection. In conclusion, the selective inhibition of IFN-_-inducible MHC class II, but not ICAM-1, by chlamydial infection may be driven by host immune selective pressure. (Abstract shortened by UMI.) en_US
dc.format.extent 5820410 bytes
dc.format.extent 184 bytes
dc.format.mimetype application/pdf
dc.format.mimetype text/plain
dc.language en en_US
dc.language.iso en_US
dc.rights info:eu-repo/semantics/openAccess
dc.title Suppression of MHC class II but not ICAM-1 molecules by chlamydial infection en_US
dc.type info:eu-repo/semantics/masterThesis
dc.type master thesis en_US
dc.degree.discipline Medical Microbiology en_US
dc.degree.level Master of Science (M.Sc.) en_US


Files in this item

This item appears in the following Collection(s)

Show simple item record

View Statistics