The clinical manifestations of hemolytic disease of the fetus and newborn mediated by anti-K, an antibody of the Kell blood group system, are distinguishable from the classical form of the disease. Affected fetuses have low numbers of circulating reticulocytes and antibody titers and bilirubin levels are not reliable predictors of anemia. These observations suggest that antibodies to Kell glycoprotein lead to anemia through suppression of erythropoiesis. This study established a liquid erythroid progenitor cell culture model in which to perform analyses on the mechanism of the suppressive growth effect of anti-Kell glycoprotein. Using this culture model, this study demonstrated the requirement for co-ligation of Kell glycoprotein by a bivalent antibody for growth suppression. The absence of markers of apoptosis in cell cultures treated with anti-Kell glycoprotein suggests that the mechanism of growth suppression is distinct from programmed cell death and necrosis. Furthermore, this growth suppression cannot be rescued by erythropoietin.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:OTU.1807/17221 |
| Date | 26 February 2009 |
| Creators | Seto, Eva |
| Contributors | Denomme, Gregory |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
| Format | 4042677 bytes, application/pdf |
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