CD4+ and CD8+ T lymphocytes both contribute to acquired immunity to blood-stage Plasmodium chabaudi AS

Podoba, John E.; Stevenson, Mary M.

doi:10.1128/iai.59.1.51-58.1991

Cited by 124 publications

(68 citation statements)

References 38 publications

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“…Second, T-cells are indispensable for acquiring immunity against blood-stage malaria as shown particularly in diverse murine malaria models such as P. chabaudi chabaudi, P. chabaudi adami, and P. yoelii (for reviews, see Weidanz & Long 1988, Good & Miller 1989, Langhorne et al 1989. Especially CD4+ T cells are of primary importance though B cells and/or CD8+ cells are also required (Jayawardena et al 1982, Meding & Langhorne 1991, Podoba & Stevenson 1991. Third, it has been reported that the adoptive transfer of T cells from immune mice does not help recipient mice to develop immunity against P. chabaudi under certain experimental conditions (McDonald & Phillips 1978, Favila-Castillo et al 1990.…”

Section: Discussionmentioning

confidence: 99%

Testosterone‐unresponsiveness of existing immunity against Plasmodium chabaudi malaria

Wunderlich

Benten

Bettenhaeuser

et al. 1992

Parasite Immunology

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Testosterone (Te) is known to suppress immunity and to increase host susceptibility to many parasites. This study investigates the action of Te on immunity acquired against blood-stages of the malaria parasite Plasmodium chabaudi in female mice of the inbred strain C57BL/10. Our data show: (i) About 90% of mice infected with 10(6) P. chabaudi-infected erythrocytes are able to develop protective immune mechanisms which become evident in self-healing the infection. The capability of self-healing is lost when mice are pretreated with Te for 3 weeks. (ii) Mice which have self-healed infections acquire immunity to homologous rechallenge. Concomitantly, mice become Te-unresponsive in that their acquired immunity is not suppressible by Te-treatment. (iii) Flow cytometry reveals that Te-pretreatment entails an increase of CD8+ cells and a decrease of Ig+ cells by about 4% in spleens of non-immune mice. In immune mice, however, there is a Te-unresponsiveness of the percental distribution of splenic cell populations. (iv) Adoptive transfer experiments indicate that immunity is conferred by spleen cells, presumably non-T-cells. These cells are Te-unresponsive, since they exert their effect in Te-pretreated mice in the presence of Te. (v) Te-unresponsive immunity can be also transferred by serum, especially the IgG-fraction, obtained from immune mice. Our data demonstrate that Te prevents the development of protective immunity against P. chabaudi infections. However, when once established, protective immunity becomes unresponsive to Te. Our data suggest that the effector mechanisms of protective immunity involve Te-unresponsive B cells secreting protective IgG-antibodies.

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Section: Discussionmentioning

confidence: 99%

Testosterone‐unresponsiveness of existing immunity against Plasmodium chabaudi malaria

Wunderlich

Benten

Bettenhaeuser

et al. 1992

Parasite Immunology

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“…Plasmodium chabaudi AS was maintained by weekly passage in C57B1/6 mice as previously described [1]. For passage or infection of experimental animals, blood was collected via the retro-orbital plexus from two infected C57B1/6 mice and pooled.…”

Section: Parasitementioning

confidence: 99%

“…The importance of CD4^ T lymphocytes in the resolution ofa primary infection with blood-stage Plasmodium chahaudi has been established by the results of studies from our laboratory and others [1][2][3][4]. It would appear that these cells function during the early or acute phase ofthe infection in mediating the rapid decrease in peak parasitaemia to low or sub-patent chronic levels via antibody-independent cell-mediated meehanisms.…”

Section: Introductionmentioning

confidence: 99%

Differential induction of helper T cell subsets during blood-stage Plasmodium chabaudi AS infection in resistant and susceptible mice

Stevenson

Tam

1993

Clinical and Experimental Immunology

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152

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The induction of T helper cell subsets during the course of non-lethal or lethal blood-stage Plasmodium chabaudi AS infection was investigated using inbred strains of mice which differ in the level of resistance to this intraerythrocytic parasite. Resistant C57Bl/6 mice experience a non-lethal course of infection characterized by moderate levels of both parasitaemia and anaemia and resolution of primary acute infection by 4 weeks, while susceptible A/J mice experience lethal infection with fulminant parasitaemia and severe anaemia. T helper subset function was assessed during infection by determining the kinetics of spleen cell production in vitro of the Th1-derived cytokine, interferon-gamma (IFN-gamma), and of the Th2-derived cytokine, IL-5, using sandwich ELISAs. Spleen cells from resistant C57Bl/6 mice were found to produce high levels of IFN-gamma within 1 week of infection in response to both the mitogen concanavalin A (Con A) and malaria antigen. Furthermore, CD4+ T cells were found to be the source of IFN-gamma while both CD4+ and CD8+ T cells were found to produce IL-5. Decreased IFN-gamma production after day 10 was concomitant with significant production of IL-5 between 2 and 3 weeks post infection. In contrast, spleen cells from susceptible A/J mice produced high levels of IL-5 within the first week of infection. In addition, these animals were found to have high serum levels of IL-5. These results, thus, confirm previous observations that resolution of primary blood-stage P. chabaudi infection occurs by sequential activation of Th1 CD4+ T cells followed by activation of the Th2 subset, and in addition, suggest that induction of a strong Th2 response early in infection may lead to a severe and lethal course of malaria.

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“…3,4 This evidence strongly indicates that malaria-specific antibodies play a crucial role in protective immunity against malaria. Previous studies using a rodent model of malaria showed that CD4 + T-cell-depleted mice fail to control Plasmodium infection, [5][6][7][8] as is the case with interferon-c (IFN-c)-signalling-deficient mice. 2,[9][10][11][12][13] IFN-c-signalling-deficient mice may exhibit decreased dendritic cell activation and T helper type 1 (Th1) responses during infection.…”

Section: Introductionmentioning

confidence: 99%

γδ T cells modulate humoral immunity against Plasmodium berghei infection

et al. 2018

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It is unclear whether γδ T cells are involved in humoral immunity against Plasmodium infection. Here, we show that B-cell-immunodeficient mice and γδ T-cell-deficient mice were incapable of protecting against Plasmodium berghei XAT parasites. γδ T-cell-deficient mice developed reduced levels of antigen-specific antibodies during the late phase of infection. The numbers of follicular helper T cells and germinal centre B cells in γδ T-cell-deficient mice were lower than in wild-type mice during the late phase of infection. Expression profiling of humoral immunity-related cytokines in γδ T cells showed that interleukin-21 (IL-21) and interferon-γ (IFN-γ) are increased during the early stage of infection. Furthermore, blockade of IL-21 and IFN-γ signalling during the early stage of infection led to reduction in follicular helper T cells and germinal centre B cells. γδ T-cell production of IL-21 and IFN-γ is crucial for the development and maintenance of follicular helper T cells and germinal centre B cells during the late phase of infection. Our data suggest that γδ T cells modulate humoral immunity against Plasmodium infection.

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CD4+ and CD8+ T lymphocytes both contribute to acquired immunity to blood-stage Plasmodium chabaudi AS

Cited by 124 publications

References 38 publications

Testosterone‐unresponsiveness of existing immunity against Plasmodium chabaudi malaria

Testosterone‐unresponsiveness of existing immunity against Plasmodium chabaudi malaria

Differential induction of helper T cell subsets during blood-stage Plasmodium chabaudi AS infection in resistant and susceptible mice

γδ T cells modulate humoral immunity against Plasmodium berghei infection

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