Suppression of MHC class II but not ICAM-1 molecules by chlamydial infection
| 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.degree.discipline | Medical Microbiology | en_US |
| dc.degree.level | Master of Science (M.Sc.) | en_US |
| 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.identifier.uri | http://hdl.handle.net/1993/2593 | |
| dc.language.iso | eng | en_US |
| dc.rights | open access | en_US |
| dc.title | Suppression of MHC class II but not ICAM-1 molecules by chlamydial infection | en_US |
| dc.type | master thesis | en_US |