The Role of Serum Immunoglobulin E in the Pathogenesis of <i>Plasmodium falciparum</i> Malaria in Ivorian Children

Seka-Seka, J.; Brouh, Y.; Yapo‐Crézoit, A. C.; Atseye, N. H.

doi:10.1111/j.0300-9475.2004.01337.x

Cited by 29 publications

(26 citation statements)

References 7 publications

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“…This was supported by a study that showed an association between polymorphisms in FccRIIa, the platelet IgG receptor and disease severity [48]. IgE levels have also been associated with severity of malaria [49] and an increase in IgM levels has also been reported [50]. IgE response to parasites and allergens has been shown to involve an IgE-mediated activation of platelets [51][52][53].…”

Section: Immune Mechanismsmentioning

confidence: 79%

The role of platelets in the pathogenesis of cerebral malaria

Cox

McConkey

2009

Cell. Mol. Life Sci.

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Malaria is a major cause of morbidity and mortality in the developing world and cerebral malaria is responsible for the majority of malaria-associated deaths. There is a strong association between thrombocytopenia and outcome in malaria, suggesting a role for platelets in the pathogenesis of malaria. This thrombocytopenia is likely due to platelet activation possibly through an interaction between PfEMP1 on plasmodium and CD36 on platelets. Platelet activation by plasmodium has two potential consequences. It can lead to the formation of micro-aggregates of infected red blood cells and platelets which can occlude blood vessels and it also leads to binding to and activation of the endothelium.

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Section: Immune Mechanismsmentioning

confidence: 79%

The role of platelets in the pathogenesis of cerebral malaria

Cox

McConkey

2009

Cell. Mol. Life Sci.

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“…Are antibodies involved in the observed malaria-induced thrombocytopenia? Most malaria patients with thrombocytopenia possess platelet-associated antibodies that bind to plateletbound malaria antigens [19], and the extent of thrombocytopenia correlates with disease severity and immunoglobulin E (IgE) levels [20]. One hypothesis is that platelet autoantibodies and subsequent phagocytosis by splenic macrophages are responsible for the observed thrombocytopenia, although in experiments with P. berghei in μMT mice (which are considered devoid of functional B cells and IgG antibodies), the mice still develop thrombocytopenia [21].…”

Section: A Spoonful Of Antibodies Makes the Platelets Go Down?mentioning

confidence: 99%

Platelet power: sticky problems for sticky parasites?

Pleass

2009

Trends in Parasitology

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Platelets might have a crucial role in the pathogenesis of both human and rodent malarias by assisting in the sequestration of infected erythrocytes within the cerebral vasculature. However, recent elegant work by McMorran et al. suggests that they are also involved in innate protection during the early stages of infection. Here, we discuss the implications of their important findings in the context of immunity to malaria. Platelet: friend or foe?The platelet, traditionally known for its role in blood clotting, is also known for its putative involvement in malaria pathology [1,2]. However, a recent study using C57BL6 mice genetically deficient in the megakaryocyte growth and differentiation factor C-mpl (encoded by the Mpl gene), and resulting in mice with 90% fewer platelets, showed that these animals were significantly more susceptible to death when infected with Plasmodium chabaudi [3]. Furthermore, the authors went on to show that purified human platelets killed Plasmodium falciparum parasites within red blood cells when added to in vitro cultures and that various platelet antagonists, including aspirin, reversed this antiparasitic activity both in vitro and in vivo. This result raises concerns over the use of aspirin as an antipyretic in patients with malaria. Using specific receptor antagonists, the authors demonstrated that killing and control of parasite growth in P. falciparum cultures was dependent on platelet activation via P2Y1, an ADP-dependent metabotrophic puronergic receptor (Figure 1).These results in animals seem counterintuitive, in that platelets are believed to be involved in pathological disease states that hasten death, such as cerebral malaria [1,2]. For example, mice with significantly compromised platelet function (CXCL4 or CXCR3 deficient) have been shown to survive longer than their wild-type counterparts [4]. By contrast, platelet depletion by anti-CD41 monoclonal antibody injection early, but not late, in the course of disease is known to protect C57BL6 mice from Plasmodium berghei ANKA-induced severe experimental cerebral malaria (ECM) by altering levels of pathogenic cytokines [5]. Unfortunately, the study by McMorran et al. used P. chabaudi, a rodent malaria thatalthough capable of sequestering to a number of organs -is not known to develop ECM. It should also be noted that non-sequestering Plasmodium species also give rise to ECM in some inbred mouse strains, Plasmodium yoelii 17XL in BALB/c mice being a good example Europe PMC Funders Group A cornucopia of receptorsThe first of these questions is easier to explain for P. falciparum than for Plasmodium vivax or the murine malarias. Platelet-mediated clumping is common in P. falciparum field isolates, is distinctive from other adhesive phenotypes and involves the host receptors CD36[7] and gC1qR/HABP1/p32 [8]. Whether these are the only platelet receptors involved is debatable and worth exploring. Although GPIIb/IIIa (CD41/CD61) and GPIb/IX (CD42a/ CD42b)-deficient platelets still clump to infected erythrocytes [7], the...

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“…20 In other studies, markedly raised levels of IgE were associated with the pathogenesis of severe malaria as IgE containing immune complexes or aggregates were shown to induce TNF-a production by monocytes and other effector cells through cross-linking of CD23 receptors. 21,22 Previous studies observed that the immune system of the pregnant woman is biased towards antibody production and away from cell-mediated immunity. 23,24 It has been suggested that Th2 cytokines (anti-inflammatory cytokines) down regulate Th1 cytokine responses (pro-inflammatory) thus protecting the foetus from rejection 25 but also increasing the incidence of several infectious diseases that are usually under control of CD4 + T lymphocytes.…”

Section: Introductionmentioning

confidence: 99%