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The antibody-dependent cellular inhibition (ADCI) assay is designed to assess the capability of antibodies to inhibit the in vitro growth of Plasmodium falciparum in the presence of monocytes. Our studies have shown that antibodies that proved protective against P. falciparum blood stages by passive transfer in humans are unable to inhibit the parasite in vitro unless they are able to cooperate with blood monocytes (1,2). It was also shown that antibodies that were not protective in vivo had no effect on P. falciparum growth in the ADCI assay (3,4). The ADCI is therefore an in vitro assay the results of which reflect the protective effect of antimalarial antibodies observed under in vivo conditions in humans. [ABSTRACT FROM AUTHOR]

Our results have emphasized the potential involvement of the antibody-dependent cellular inhibition (ADCI) mechanism in the protective effect of antibodies mediating acquired immunity to Plasmodium falciparum malaria (1). The ADCI mechanism consists of a cooperation between monocytes and cytophilic antibodies able to bind to the Fc receptors present on the monocyte surface. Thus human IgG1 and IgG3 are the main isotypes effective in ADCI, whereas IgG2, IgG4, and IgM are ineffective and could rather have a blocking effect if they are directed to parasite antigens that are targets of effective antibodies (2-4). Therefore, in order to assess the potential role of a given parasite antigen in triggering protective immune responses, it is of interest to characterize the isotype distribution of antibodies directed to this antigen and elicited in protected versus nonprotected individuals. [ABSTRACT FROM AUTHOR]