A role of IgE and CD23/NO immune pathway in age-related resistance of Lewis rats to Plasmodium berghei Anka?

Safeukui, Innocent; Vatan, Rémi; Dethoua, Mariette; Agbo, Hervé; Haumont, Gilbert; Moynet, Daniel; Malvy, Denis; Vincendeau, Philippe; Mossalayi, Djavad; Millet, Pascal

doi:10.1016/j.micinf.2008.07.033

Cited by 6 publications

(5 citation statements)

References 20 publications

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“…Our data suggest that following T. gondii infection, macrophages acquire simultaneously CD23 signaling and the availability of IgE-IC, their natural ligands. Previous studies conducted in various parasitic and microbial infections have shown CD23 expression together with its role in intracellular and extracellular killing of pathogens by macrophages [3], [8], [10]. Cell activation via CD23 requires the presence of appropriate physiologic ligands [25] such as immunoglobulin E, CD21, CD11b/c, CD47-vitronectin, and mannose-containing proteins [7].…”

Section: Discussionmentioning

confidence: 99%

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IgE Mediates Killing of Intracellular Toxoplasma gondii by Human Macrophages through CD23-Dependent, Interleukin-10 Sensitive Pathway

et al. 2011

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BackgroundIn addition to helminthic infections, elevated serum IgE levels were observed in many protozoal infections, while their contribution during immune response to these pathogens remained unclear. As IgE/antigen immune complexes (IgE-IC) bind to human cells through FcεRI or FcεRII/CD23 surface molecules, the present study aimed to identify which functional receptor may be involved in IgE-IC interaction with human macrophages, the major effector cell during parasite infection.Methodology/Principal FindingsHuman monocyte-derived macrophages were infected with Toxoplasma gondii before being incubated with IgE-IC. IgE receptors were then identified using appropriate blocking antibodies. The activation of cells and parasiticidal activity were evaluated by mediator quantification and direct counting of infected macrophages. RNAs were extracted and cell supernatants were also collected for their content in tumor necrosis factor (TNF)-α, interleukin-10 (IL-10) and nitrites. Sera from symptomatic infected patients were also tested for their content of IgE, IL-10 and nitrites, and compared to values found in healthy donors. Results showed that IgE-IC induced intracellular elimination of parasites by human macrophages. IgE-mediated effect was FcεRI-independent, but required cross-linking of surface FcεRII/CD23, cell activation and the generation of nitric oxide (NO). Although TNF-α was shown to be produced during cell activation, this cytokine had minor contribution in this phenomenon while endogenous and exogenous IL-10 down-regulated parasite killing. Inverse relationship was found between IL-10 and NO expression by infected human macrophages at both mRNA and mediator levels. The relationship between these in vitro data and in vivo levels of various factors in T. gondii infected patients supports the involvement of CD23 antigen and IL-10 expression in disease control.ConclusionThus, IgE may be considered as immune mediator during antiprotozoal activity of human macrophages through its ability to trigger CD23 signaling. Increased cell activation by IgE-IC may also account for chronic inflammatory diseases observed in some patients.

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Section: Discussionmentioning

confidence: 99%

“…Thus, in vivo expression of IgE has been observed during protozoal infections such as those caused by Plasmodium spp. [2], [3], Leishmania spp. [4] and Trypanosoma cruzi [5], although the role of this immunoglobulin in anti-microbial immunity remains unclear [6].…”

Section: Introductionmentioning

confidence: 99%

IgE Mediates Killing of Intracellular Toxoplasma gondii by Human Macrophages through CD23-Dependent, Interleukin-10 Sensitive Pathway

et al. 2011

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“…During various parasitic infections, increased expression of this molecule has been observed. Its role in the generation of microbicidal mediators from macrophages and in intracellular and extracellular killing of pathogens has been described (29,40,48). Since both gamma interferon (IFN-␥) and IL-4 are able to promote CD23 gene expression, this pathway could be involved during both Th1 and Th2 responses (20,35).…”

Section: Discussionmentioning

confidence: 99%

CD23 Mediates Antimycobacterial Activity of Human Macrophages

et al. 2009

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“…There is conflicting evidence regarding the role of NO in the process of resistance against malaria parasites. Schizonts treated in vitro with NO donors caused a delayed infection to mice in a dose and time-dependent manner, which, suggest an inhibitory role for NO [58] with influence on parasitemia and survival of Plasmodium berghei in infected mice [59] or P. berghei Anka in rats [60]. Moreover, human severe malaria is associated with decreased NO production [61] and iNOS variants in regions of differing disease manifestation [62].…”

Section: Plasmodium Spmentioning

confidence: 95%

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

Nahrevanian

2009

Braz J Infect Dis

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Nitric oxide (NO) is a potent mediator with diverse roles in regulating cellular functions and signaling pathways. The NO synthase (NOS) enzyme family consists of three major isoforms, which convey variety of messages between cells, including signals for vasorelaxation, neurotransmission and cytotoxicity. This family of enzymes are generally classified as neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Increased levels of NO are induced from iNOS during infection; while eNOS and nNOS may be produced at the baseline in normal conditions. An association of some key cytokines appears to be essential for NOS gene regulation in the immunity of infections. Accumulating evidence indicates that parasitic diseases are commonly associated with elevated production of NO. NO plays a role in the immunoregulation and it is implicated in the host non-specific defence in a variety of infections. Nevertheless, the functional role of NO and NOS isoforms in the immune responses of host against the majority of parasites is still highly controversial. In the present review, the role of parasitic infections will be discussed in the controversy related to the NO production and iNOS gene expression in different parasites and a variety of experimental models.

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A role of IgE and CD23/NO immune pathway in age-related resistance of Lewis rats to Plasmodium berghei Anka?

Cited by 6 publications

References 20 publications

IgE Mediates Killing of Intracellular Toxoplasma gondii by Human Macrophages through CD23-Dependent, Interleukin-10 Sensitive Pathway

IgE Mediates Killing of Intracellular Toxoplasma gondii by Human Macrophages through CD23-Dependent, Interleukin-10 Sensitive Pathway

CD23 Mediates Antimycobacterial Activity of Human Macrophages

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

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