IgE elevation and IgE anti-malarial antibodies in <i>Plasmodium falciparum</i> malaria; association of high IgE levels with cerebral malaria

Perlmann, Hedvig; Helmby, Helena; Hagstedt, Margareta; Carlson, Jonathan O.; Larsson, Peter; Troye‐Blomberg, Marita; Perlmann, Peter

doi:10.1111/j.1365-2249.1994.tb06082.x

Cited by 113 publications

(61 citation statements)

References 49 publications

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“…IgE antibodies may protect against, or participate in, the pathogenesis of malaria. The association of high anti-P. falciparum IgE levels with a reduced risk of developing clinical malaria suggests a protective role [13], whereas the observation that circulating levels of IgE most often correlate with severe rather than uncomplicated disease suggests a pathogenic role [14]. Recently, Duarte et al [15] have reported that circulating levels of total IgE do not appear to correlate with protection or pathology during malaria.…”

Section: Discussionmentioning

confidence: 99%

Mast cell‐mediated immune responses through IgE antibody and Toll‐like receptor 4 by malarial peroxiredoxin

et al. 2008

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In this study, 2-Cys Plasmodium berghei ANKA (PbA) peroxiredoxin (Prx) was identified as an antigenic protein recognized by an anti-PbA IgE antibody using two-dimensional polyacrylamide gel electrophoresis and proteomic analysis. Innate immune responses to PbAPrx were examined using cells from mice deficient in Toll-like receptors (TLR) or related molecules, and it was demonstrated that responses were severely impaired in TLR4 -/-, MyD88 -/-and MD-2 -/-mice, but not in Toll/IL-1 receptor domain-containing adaptor inducing IFN-c (TRIF) -/-, TLR2 -/-or radioprotective 105 (RP105) -/-mice. An association between PbAPrx and TLR4 was observed following immunoprecipitation and immunoblotting, suggesting that PbAPrx was associated with TLR4/MD-2. Interactions between Prx and TLR4/MD-2 were also examined by flow cytometry using TLR4/MD-2-or TLR2-expressing cells. NFjB/GFP activity was observed in TLR4/MD-2-but not in TLR2-expressing cells following stimulation with Prx. However, this effect was not observed after treatment with proteinase K, suggesting that PbAPrx is a protein ligand for TLR4 and that the PbAPrx activity observed in this study is not due to contamination with LPS. These findings indicate that malarial Prx induces IgE-mediated protection through FceRI on mast cells and innate immunity through TLR4 with MyD88 and MD-2, suggesting a novel function for malarial Prx in innate and acquired immune responses in malaria.

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Section: Discussionmentioning

confidence: 99%

Mast cell‐mediated immune responses through IgE antibody and Toll‐like receptor 4 by malarial peroxiredoxin

et al. 2008

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“…These IgE antibodies are produced from the Th-2 immune response and have been used in serodiagnosis and also as indicator of the disease activity in many diseases such as toxoplasmosis, cerebral malaria, and visceral leishmaniasis (Wong et al 1993;Perlmann et al 1994;Atta et al 1998).…”

Section: Anti Leishmanial Ige Antibodymentioning

confidence: 99%

Comparative immune study on cutaneous leishmaniasis patients with single and multiple sores

2013

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Ninety-five Iraqi patients with cutaneous leishmaniasis (CL) caused by Leishmania tropica at AL-Karama Hospital in Baghdad were included in this study. Sixty patients were with single sore and the remaining with multiple sores. The study also included 10 atopic patients and 30 healthy individuals as a control group. Cellular and humoral immune response at different stages of the disease activity (early and late) were evaluated by estimation of serum IFNc, IL-4 and total IgE antibodies using ELISA kits while, the detection of specific anti leishmanial IgE antibodies was done manually. Specific IgE antibodies were only detected in early CL (\2 months) patients 68 (71.57 %) while, were not detected in late CL, atopic and healthy controls 30 (100 %). The results also showed a positive relationship between this antibody and the number of sores. Th-2 predominates during the early stage of the disease then shifts to Th-1 that proceed in the late stage, but both cytokines increased in CL patients in comparison to control group. The immune response of CL infection is possibly regulated by both Th-1 and Th-2. Multiple sores patients showed an increase of anti leishmanial IgE (0.120 ± 0.014), total IgE (120.7 ± 39.58 IU/ml), IFN-c (87.4 ± 30.52 pg/ml) and IL-4 (63.70 ± 20.32 pg/ml) levels than single sore patients with mean value of 0.108 ± 0.14, 92.3 ± 35.23 IU/ml, 47.2 ± 27.80 pg/ml and 51.04 ± 15.0 pg/ml respectively. It can be presented also as ratio of INF-c/IL-4 = 1.37 which is greater than those for single sore 0.9. These results indicated that the immune response of multiple sores patient's is higher than that with single sores.

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“…In addition, with repeated exposure to Plasmodium spp., an immune response repertoire, chiefl y consisting of cytophilic IgG1 and IgG3 subclasses, but also IgE, will progressively evolve in children, having the capacity to control and reduce parasite multiplication [9,[20][21][22]. Such responses may gradually approach, and come to resemble, the immune reactivity profi les observed in adults, where antibodies specifi c against multiple P. falciparum antigens mediate partial parasite control [23].…”

Section: Introductionmentioning

confidence: 99%

“…The initial fi nding indicated that IgE elevation was most pronounced in sera from patients with cerebral malaria [22]. Later observations suggested that IgE may be considered a pathogenic factor in severe disease without cerebral involvement and, probably, in P. falciparum malaria in general [24].…”

Section: Introductionmentioning

confidence: 99%

Chemokine levels and parasite- and allergen-specific antibody responses in children and adults with severe or uncomplicatedPlasmodium falciparummalaria

Wangala¹,

Vovor²,

Gantin³

et al. 2015

European Journal of Microbiology and Immunology

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Chemokine a nd antibody response profiles were investigated in children and adults with severe or uncomplicated Plasmodium falciparum malaria; the aim was to reveal which profiles are associated with severe disease, as often seen in nonimmune children, or with mild and uncomplicated disease, as seen in semi-immune adults. Blood samples were obtained from children under 5 years of age as well as adults with falciparum malaria. Classification of malaria was performed according to parasite densities and hemoglobin concentrations. Plasma levels of chemokines (IL-8, IP-10, MCP-4, TARC, PARC, MIP-1δ, eotaxins) were quantified, and antibody responses (IgE, IgG1, and IgG4) to P. falciparum, Entamoeba histolytica-specific antigen, and mite allergen extracts were determined. In children with severe malaria proinflammatory, IL-8, IP10, MIP-1δ, and LARC were at highly elevated levels, suggesting an association with severe disease. In contrast, the Th2-type chemokines TARC, PARC, and eotaxin-2 attained in children the same levels as in adults suggesting the evolution of immune regulatory components. In children with severe malaria, an elevated IgG1 and IgE reactivity to mite allergens and intestinal protozoan parasites was observed. In conclusion, exacerbated proinflammatory chemokines together with IgE responses to mite allergens or E. histolytica-specific antigen extract were observed in children with severe falciparum malaria.

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IgE elevation and IgE anti-malarial antibodies in Plasmodium falciparum malaria; association of high IgE levels with cerebral malaria

Cited by 113 publications

References 49 publications

Mast cell‐mediated immune responses through IgE antibody and Toll‐like receptor 4 by malarial peroxiredoxin

Mast cell‐mediated immune responses through IgE antibody and Toll‐like receptor 4 by malarial peroxiredoxin

Comparative immune study on cutaneous leishmaniasis patients with single and multiple sores

Chemokine levels and parasite- and allergen-specific antibody responses in children and adults with severe or uncomplicatedPlasmodium falciparummalaria

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