Michel Jc

Opsonic activity of ascitic fluids from Plasmodium falciparum-infected Saimiri monkey: Positive correlation with protection in passive transfer assay

An investigation into the protective activity of ascitic fluids from Saimiri monkeys infected with Plasmodium falciparum and the role played by opsonins in that activity was undertaken. P. falciparum-parasitized blood was collected from splenectomized Saimiri (when parasitaemia reached at least 20% or more) and used in an in vitro phagocytic assay including ascitic fluid and cultures of peripheral blood monocytes from normal Saimiri. Under the conditions of this in vitro assay, we found that ascitic fluid phagocytosis-promoting factors were opsonic rather than cytophilic. The opsonic activity was highly specific for parasitized red blood cells and was effective against all stages of development of the parasite. A highly positive relationship between in vitro opsonizing activity and in vivo protective capacity of immune ascitic fluid was found.

Incidence d'une réaction inflammatoire sur la résistance des souris envers Plasmodium berghei

Abstract An inflammatory reaction induced in mice by a subcutaneous injection of magnesium silicate embedded in a calcium phosphate gel is followed by an increased resistance against Plasmodium berghei . The occurrence of this increased resistance is related to the time elapsed between the induction of the inflammatory process and the infection. The delayed mortality is correlated with a slowed development of parasitemia. It is hypothesized that the protective effect may be related to the capacity of the inflammatory reaction to promote in mice both specific and non-specific antiparisitic immune responses.

Modulation by malaria infection of the induction of T lymphocyte-dependent delayed-type hypersensitivity and antibody formation to sheep erythrocytes in mice.

Summary A profound alteration of the inductive phase of delayed‐type hyper‐sensitivity and antibody formation to SRBC was found in malaria infected mice when sensitization with this antigen was performed intravenously at a critical time of the disease, but not after subcutaneous immunization, suggesting a major role for the spleen in the mechanism of immunodepression.