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Elsaid, Hassan Mohamed 1988 Immune Recognition of Parasite-Dependent Antigens associated with Plasmodium Falciparum - Infected Erythrocytes, PhD Dissertation, Michigan State University

    © Hassan Mohamed Elsaid, 1988. Use of any part of this thesis for any purpose must be acknowledged.


The intraerythrocytic infection of Plasmodium falciparum constitutes the primary mechanism by which the parasite evades recognition by human immune mechanisms. In this study we investigated the ability of human immune sera and peripheral blood monocytes to recognize erythrocytes infected with this parasite. Sera from adults living in malaria endemic areas of Sudan, Nigeria and Irian Jaya contained immunoglobulins specific for parasite-dependent antigens expressed on infected, but not non-infected, erythrocytes. Six in vitro-adapted parasite strains of different phenotypes, regarding expression of knob structures and cytoadherence affinity to human endothelium/C32 melanoma cells, showed diverse antigenic repertoires on infected erythrocytes. The differences in levels of recognition of individual strains correlated with the drift from knobby and endothelium-binder to knobless and endothelium-non-binder phenotypes. The expression of knob structures alone on erythrocyte surface was not sufficient for conferring antigenicity or cytoadherence ability to infected erythrocytes. Two strains failed to react with any of the sera employed in the study. These parasites may display a rare antigenic repertoire or completely lost expression of erythrocyte surface antigens. Sera that opsonized infected erythrocyte surface could also inhibit their cytoadherence to human C32 melanoma cells. Endothelium-binder parasites may express determinants common to the different isolates of the parasite, or immune sera may contain a mixture of immunoglobulin specificities directed at distinct epitopes expressed on antigenically diverse isolates, however, associated with the cytoadherence molecules on infected erythrocytes. Human peripheral blood monocytes were unable to recognize infected erythrocytes, as indicated by their inability to phagocytose the infected targets. In the presence of immunoglobulin molecules specific for erythrocyte surface antigens, monocytes could recognize, bind and phagocytose infected erythrocytes. Primary infection sera were devoid of reactivity to infected erythrocyte surface, although specificity for parasite antigens was evident in both IgG and IgM immunoglobulin classes. Although parasite-dependent antigens on surface of infected erythrocytes may be variant, they apparently elicit specific antibodies, and for infection with a given parasite, probably play a major role in controlling rising parasitemia.


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