Antibody-complement interaction with lipid model membranes.
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Biomedical subjects
Publications and source records attributed to S C Kinsky.
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Liposomes containing trapped glucose marker were prepared from the chloroform-soluble fraction of sheep erythrocyte membranes. These liposomes release glucose when incubated with rabbit anti-sheep erythrocyte serum and a source of complement. Experiments with purified human complement components show that loss of marker is absolutely dependent on the presence of components 2 and 8. An absolute requirement for component 9 cannot be demonstrated, although it stimulates glucose release from the liposomes. These results establish a parallelism between the response of biological membranes and liposomal membranes to antibody and complement.
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Incorporation of lipid A influences the immunogenic properties of liposomal model membranes that carry N-(hapten)-substituted derivatives of phosphatidylethanolamine as antigenic determinants. These effects of lipid A include a marked enhancement of the hapten-specific response; abolition of the requirement of critical threshold epitope density for liposomal immunogenicity; and conversion of liposomes from a thymus-independent type 2 to a thymus-independent type 1 immunogen. Recent experiments demonstrate that an optimal in vitro response to liposomes--although originally classified as thymus-independent on the basis of conventional criteria--requires two T cell factors, interleukin-2 and interleukin-X, which are also involved in the response to a classic thymus-dependent immunogen. Incorporation of lipid A has no qualitative effect on the dependence of liposomal immunogenicity on these lymphokines.