T-cell activation in murine malaria

Jayawardena, Anil N.; Targett, G. A. T.; Leuchars, E.; Carter, R. L.; Doenhoff, Michael J.; Davies, A. J. S.

doi:10.1038/258149a0

Cited by 81 publications

(30 citation statements)

References 9 publications

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“…A role of T cells in immunosuppression during P. berghei infection was also evidenced on studying the specific and non-specific delayed-type hypersensitivity responses in the in vivo system (10). Similar findings have been previously reported by other workers during acute infection (6,7,9,11). Therefore it became necessary to make a quantitative estimation of subsets of T lymphocytes which participate in immunosuppression during acute and chronic P. berghei infection.…”

Section: Discussionsupporting

confidence: 93%

“…Alteration of the lymphocytes number in the thymus, lymph nodes, spleen and blood have been reported during malaria infection (3)(4)(5). A rapid loss in responsiveness of T cell mitogen (phytohaemagglutinin, PHA) has been shown in spleen cells of mice infected with Plasmodium berghei or Plasmodium yoelii (6,7). Maximal suppression in P. yoelii infection occurs at peak parasitaemia.…”

Section: Introductionmentioning

confidence: 99%

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Quantitative estimation of suppressor/cytotoxic and helper T cells during acute and chronic Plasmodium berghei infection

Wangoo

Kaur

Ganguly

et al. 1990

Immunology & Cell Biology

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SummaryIn the present study, the percentage of lymphocyte subpopuiations and their relation to T cell subsets was estimated during acute and chronic Plasmodium berghei malaria. During acute infection, a decreased percentage of T lymphocytes was observed, whereas no change was observed during chronic infection. However, no change in the percentage of B cells was observed in both types of infection. The T cell population was characterized by an increased percentage of T suppressor cytotoxic (CD8+) cells and a decreased percentage of T helper cells (CD4+) during acute infection. This resulted in an inversion ofthe CD8+/CD4+ cell ratio. During chronic infection no change in the CD8'*" cell percentage was observed; however some increase in CD4+ cell percentage was observed in later stages. Thus failure ofthe immune system to overcome acute infection may be due to an increase in T suppressor cells, and maintenance of parasites at subpatent levels during chronic infection may involve the normal CD8+/CD4+ cell ratio with some increase in CD4+ cells.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Quantitative estimation of suppressor/cytotoxic and helper T cells during acute and chronic Plasmodium berghei infection

Wangoo

Kaur

Ganguly

et al. 1990

Immunology & Cell Biology

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“…It was reported that, during self-resolving blood-stage malaria infections, there was a strong T-cell activation, which was absent in lethal infections (Jayawardena et al 1975). This notion arose first from a series of studies on the induction of Th subsets during the course of nonlethal or lethal blood-stage P. chabaudi AS infection using inbred strains of mice.…”

Section: Discussionmentioning

confidence: 98%

Cytokine and antibody production during the course of resolution in Plasmodium yoelii 17XL-infected BALB/c mice treated with febrifugine and isofebrifugine mixture from leaves of Hydrangea macrophylla var. Otaksa

et al. 2004

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Cytokine and antibody production was investigated during the course of resolution of primary infection in Plasmodium yoelii 17XL-infected BALB/c mice treated with a mixture of febrifugine and isofebrifugine. The infected mice in an untreated control group showed a progressively increasing parasitemia, leading to mouse death. In contrast, infected mice given the mixture orally showed low parasitemia levels during administration. Following a transient increase in parasitemia in the bloodstream of the treated mice, no parasites could be detected by microscopic examination. Analysis of cytokines in plasma showed that the plasma IFN-gamma levels elevated significantly within the first week of infection in both groups. Furthermore, on day 20 the plasma IFN-gamma and IL-4 levels elevated significantly in the treated mice and the production of both cytokines was sustained until at least day 40. The production of both cytokines in the treated mice was coincident with a decrease in parasitemia. The production of parasite-specific antibodies in the course of P. yoelii 17XL infection was also monitored. In the drug-treated mice, the titers of parasite-specific IgG1, IgG2a, IgG2b and IgG3 elevated significantly from day 20; and the production of parasite-specific antibodies was coincident with a decrease in parasite numbers in the bloodstream.

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“…Early studies in P. falciparum-infected children (Greenwood et al 1972) suggested that immunosuppression resulting from malarial infection seemed to have no in¯uence on the cell-mediated immune response, whereas mice-infected with the lethal parasite P. berghei demonstrated a suppression of contact hypersensitivity (Jayawardena et al 1975) and patients with P. falciparum malaria showed a reduced immune response after vaccination (Williamson and Greenwood 1978) and a reduced delayed-type hypersensitivity response (Kremsner et al 1990). Most studies addressing the eect of hemozoin on immunity have pointed in the same direction (Morakote and Justus 1988;Schwarzer et al 1992;Fiori et al 1993;Turrini et al 1993;Taramelli et al 1995;Prada et al 1996a;Pichyangkul et al 1994) Hemozoin-induced impairment of human and murine macrophages manifesting as an inhibition of further phagocytosis (Schwarzer et al 1992) and as a reduction in the production of free radicals (Schwarzer et al 1992;Taramelli et al 1995;Prada et al 1996a) has been demonstrated in in vitro experiments with pigment derived from dierent malarial parasites.…”

Section: Discussionmentioning

confidence: 97%

Protection of mice previously infected with Plasmodium vinckei against subsequent Salmonella enteritidis infection is associated with nitric oxide production capacity

Lehman

Prada

Kremsner

1997

Parasitology Research

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When mice previously cured of a Plasmodium vinckei infection were subsequently infected with Salmonella enteritidis the course of bacterial infection was significantly retarded, showing increased survival duration as compared with control infections in naive mice. Moreover, on stimulation with lipopolysaccharide and/or interferon-gamma, spleen cells from malaria-cured mice showed an increased capacity to produce tumor necrosis factor, interleukin 6, and reactive nitrogen intermediates as compared with spleen cells from naive mice. However, no significant variation in the capacity of spleen cells to release reactive oxygen intermediates was observed between previously malarious and naive mice. The most significant increases were observed in the capacity for reactive nitrogen intermediate production after P. vinckei malaria. These results suggest that the observed protection of mice against salmonellosis in the convalescent phase after malaria may be mediated by nitric oxides.

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T-cell activation in murine malaria

Cited by 81 publications

References 9 publications

Quantitative estimation of suppressor/cytotoxic and helper T cells during acute and chronic Plasmodium berghei infection

Quantitative estimation of suppressor/cytotoxic and helper T cells during acute and chronic Plasmodium berghei infection

Cytokine and antibody production during the course of resolution in Plasmodium yoelii 17XL-infected BALB/c mice treated with febrifugine and isofebrifugine mixture from leaves of Hydrangea macrophylla var. Otaksa

Protection of mice previously infected with Plasmodium vinckei against subsequent Salmonella enteritidis infection is associated with nitric oxide production capacity

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