Cellular Immunity to Malaria and Babesia Parasites: A Personal Viewpoint

Allison, A. C.

doi:10.1007/978-1-4684-4571-8_12

Cited by 15 publications

(9 citation statements)

References 88 publications

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“…Even if T cells do not have an effector role against the asexual blood stages of the malaria parasite, acquired immunity is based on the recognition of parasite antigens by the immune system, and thus T cells must be important for the development and execution of malaria immunity through the regulation of monocyte/ macrophage activation as well as through antibody production. Furthermore, other studies have indicated that cytotoxic T cells may well have an effector role against the liver stages ofa The role of NK cells and ADCC cells in malaria has been debated [1,9,30], We have previously shown that natural killer activity is enhanced by SPag activation of PBMC [26], To test whether NK cells or ADCC cells could mediate parasite killing, freshly isolated PBMC were added to P. falciparum-infected heterologous RBC, Although the PBMC were cytotoxic to the NK cell-sensitive cell line K562 and although this cytotoxicity could be enhanced by a-interferon we did not find any cytotoxicity against parasitized RBC even in the presence of a-interferon or immune serum. Although several species of interferon are capable of activating NK cells, a-interferon was chosen for these experiments as this molecule is more stable than -yfcinterferon and is thus well suited for NK activation in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…Both neutrophils and monocytes have been shown to inhibit the growth of P. falciparum in vitro [4,16,23], and several effector mechanisms appear to be responsible for this inhibition. Thus both cell types have been shown to phagocytize infected erythrocytes [18,19], and to generate soluble products toxic to the parasites [6,23], Although Coleman et al [8] showed that spleen cells from mice can be cytotoxic to P. bergheiinfected red cells, the role of cytotoxic cells (natural killer (NK) cells, antibody dependent cytotoxic (ADCC) cells, T^^^.^i, cells) as effector cells in malaria is still debated [1,9,30], However, acquired immunity is based upon the recognition of the parasite by antigen-specific cells, and we have previously reported expanded T-cell clones recognizing immunosorbantpurified soluble P. falciparum antigens (SPag) in malaria-immune individuals from West Africa [25]. The present study describes the effector functions associated with these cells.…”

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confidence: 99%

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Cell‐Mediated Immunity to Plasmodium falciparum Infection: Evidence against the Involvement of Cytotoxic Lymphocytes

et al. 1988

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Blood mononuclear cells (PBMC) recognizing soluble malaria antigens (SPag) are present in the peripheral blood of individuals clinically immune to malaria, and they proliferate after exposure to such antigens. To test whether these cells have effector activity against Plasmodium falciparum, we stimulated PBMC from malaria-immune donors by SPag and purified protein derivative (PPD) in culture for 7 days. The PBMC were then co-incubated with P. falciparum for 48 h, and parasitaemia was determined by microscopy. Parasite growth was only significantly impaired after incubation with PBMC stimulated by either SPag or PPD in the presence of immune serum. Studies on subpopulations of PBMC indicated that the inhibitory cells resided among the adherent cell fraction. Furthermore we tested PBMC for cytotoxic activity against P. falciparum-infected autologous or heterologous erythrocytes. Experiments were done both in the absence and the presence of immune serum. Neither fresh PBMC nor PBMC activated by SPag or PPD for 7 days prior to assay were cytotoxic, indicating that cytotoxic T cells, natural killer (NK) cells, and K cells did not possess cytotoxic activity directed against parasitized erythrocytes. These data support the hypothesis that activated monocytes are the most important effector cells in the peripheral blood of malaria immune individuals.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Cell‐Mediated Immunity to Plasmodium falciparum Infection: Evidence against the Involvement of Cytotoxic Lymphocytes

et al. 1988

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“…Furthermore, other mechanisms such as toxic haem and generation of active oxygen radicals have been implicated in the resistance of HbAS erythrocytes lo falciparum malaria [4,5]. Allison [6] proposed ihat the protective effect of the sickle haemoglobin is acting in synergy with specific acquired immunity, and Bayoumi [7) suggested that the selective advantage of HbAS individuals is due to earlier acquisition of clinical immunity.…”

Section: Introductionmentioning

confidence: 99%

Modulation of the cellular immune response during Plasmodium falciparum infections in sickle cell trait individuals

Abu-Zeid

Theander

Abdulhadi

et al. 1992

Clinical and Experimental Immunology

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SUMMARY Plasma and peripheral blood mononuclear cells (PBMC) were obtained from P. falciparum‐infecled individuals with and without the sickle cell trait at diagnosis and 7 days after treatment. I lbAA and HbAS patients were compared for levels of plasma soluble IL‐2 receptors (IL‐2R) and the in vitro cellular reactivity to affinity‐purified soluble P. falciparum antigens (SPAg). PPD and phytohae‐magglutinin (PHA). At diagnosis. HbAS patients with clinical disease had lower plasma‐soluble IL‐2R levels and parasite counts than the corresponding HbAA patients, whereas HbAS and HbAA patients with asymptomatic infections had comparable soluble IL‐2R levels and parasite counts. PBMC from HbAS patients had higher proliferation and IFN‐γ production in response to SPAg than PBMC from HbAA patients. The difference in the lymphoproliferativc responses to SPAg between the two groups was evident in patients with asymptomatic infections. In all patients, the clinical severity, the soluble IL‐2R levels and the parasite counts were directly related. The former two were inversely related to the proliferative responses to SPAg. After treatment, all the studied parameters were comparable in the two groups. The study indicates that during P. falciparum infection, HbAS compared with HbAA patients had lower in vivo cellular activation and higher in vitro cellular reactivity in response to soluble malaria antigens.

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“…This observation may be related to a difference in the quality (avidity) of antibodies raised in the two groups of monkeys. Alternatively, it may be that the 41-kD antigen is more efficient in its native form as inducer of cell mediated responses important for the control of malaria infection (19).…”

Section: Discussionmentioning

confidence: 99%

Immunization with a Plasmodium falciparum merozoite surface antigen induces a partial immunity in monkeys.

Perrin¹,

Merkli²,

Gabra³

et al. 1985

J. Clin. Invest.

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Saimiri monkeys immunized with a Plasmodium falciparum merozoite polypeptide of 41 kD mol wt are resistant to a blood challenge infection that induces a fulminant infection in control monkeys. The sera of the immunized monkeys reacted, as shown by the indirect immunofluorescence technique, with the apical part of the merozoites from five isolates or clones of P. falciparum. Whether the immunogen was dissolved in nonionic detergent (NP-40) or in sodium dodecyl sulfate (SDS) had a marked influence on the level of protection in immunized monkeys. Thus, monkeys immunized with the antigen solubilized in a nonionic detergent developed much lower parasitemia than monkeys immunized with denatured antigen (antigen eluted from SDS polyacrylamide gel electrophoresis).

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Cellular Immunity to Malaria and Babesia Parasites: A Personal Viewpoint

Cited by 15 publications

References 88 publications

Cell‐Mediated Immunity to Plasmodium falciparum Infection: Evidence against the Involvement of Cytotoxic Lymphocytes

Cell‐Mediated Immunity to Plasmodium falciparum Infection: Evidence against the Involvement of Cytotoxic Lymphocytes

Modulation of the cellular immune response during Plasmodium falciparum infections in sickle cell trait individuals

Immunization with a Plasmodium falciparum merozoite surface antigen induces a partial immunity in monkeys.

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