Involvement of FcϵRII/CD23 and L-Arginine Dependent Pathway in IgE-Mediated Activation of Human Eosinophils

Arock, Michel; Legoff, L.; Bécherel, P.A.; Dugas, Bernard; Debré, Patrice; Mossalayi, M. Djavad

doi:10.1006/bbrc.1994.2177

Cited by 38 publications

(27 citation statements)

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“…Lantero et al [84] reported that the IgE-mediated stimulation of eosinophils from atopic and non-atopic patients by FceRII leads to functional changes characterized by the increased migration of eosinophils associated with the increased LFA-1 (lymphocyte function-associated antigen 1) and Mac-1 (macrophage-1 antigen) expression. Arock et al [85] demonstrated that the activation of Fce-RII causes the release of TNF-a by eosinophils, in which the participation of IL-4 is significant. The expression of this receptor depends on the stimulation of IL-3 and GM-CSF [86].…”

Section: Mechanisms Of Omalizumab Effect On Eosinophilsmentioning

confidence: 99%

The Effect of Omalizumab on Eosinophilic Inflammation of the Respiratory Tract in Patients with Allergic Asthma

Kupryś‐Lipińska¹,

Molińska²,

Kuna³

2016

Advances in Respiratory Medicine

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Bronchial asthma is characterised by high levels of immunoglobulin E (IgE) and overproduction of pro-inflammatory cytokines, including interleukins IL-4, IL-13 and IL-5 needed for, amongst other things, the production of IgE and the differentiation, maturation, migration and survival of eosinophils. Eosinophils are one of the most important cells in allergic inflammation. Their presence in tissue is linked to the persistence of inflammatory infiltrate, tissue damage and remodelling. Although these cells are very sensitive to corticosteroids, some asthmatic patients do not respond to high doses of these drugs, even when administered systemically. Transbronchial biopsies and bronchoalveolar lavage performed in patients with steroid-resistant asthma have demonstrated higher levels of eosinophils and Th2-type cytokines (IL-4 and IL-5) compared to steroid-sensitive patients. Clinical studies have confirmed that the very effective treatment in these cases is therapy with omalizumab -an anti-IgE monoclonal antibody. The paper discusses the efficacy of omalizumab in reducing eosinophil number in peripheral blood and in the airways of asthmatic patients based on basic, clinical, observational studies and case reports. The significance of omalizumab therapy in asthma control and mechanisms that regulate the effects of omalizumab on eosinophils are evaluated.

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Section: Mechanisms Of Omalizumab Effect On Eosinophilsmentioning

confidence: 99%

The Effect of Omalizumab on Eosinophilic Inflammation of the Respiratory Tract in Patients with Allergic Asthma

Kupryś‐Lipińska¹,

Molińska²,

Kuna³

2016

Advances in Respiratory Medicine

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“…Although eosinophils also display other IgE receptors, such as FceRI and Mac-2/ebp, it appears that many IgEinduced eosinophil functions are mediated mainly by FceRII/CD23 [9]. In addition, the demonstration that, in atopic patients, greater LFA-1 expression corresponds to disease severity and to higher serum levels of allergenspecific IgE [8] further supports the hypothesis of a significant role of FceRII in allergic asthma.…”

Section: Discussionmentioning

confidence: 81%

“…Besides inflammatory mediators, stimulation of surface receptors specific for immunoglobulins (Igs) also plays a significant role in modulating cell function [9,10]. Eosinophils are able to bind IgE through highand low-affinity receptors (FceRI and FceRII or CD23 respectively) [11,12], and, although the specific functions of FceRI and FceRII are still controversial [10,12], it has been demonstrated that anti-CD23 monoclonal antibodies (Mabs) or IgE/anti-IgE immune complexes are able to increase hydrogen peroxide and tumour necrosis factor production by eosinophils [9].…”

mentioning

confidence: 99%

“…Eosinophils are able to bind IgE through highand low-affinity receptors (FceRI and FceRII or CD23 respectively) [11,12], and, although the specific functions of FceRI and FceRII are still controversial [10,12], it has been demonstrated that anti-CD23 monoclonal antibodies (Mabs) or IgE/anti-IgE immune complexes are able to increase hydrogen peroxide and tumour necrosis factor production by eosinophils [9]. The observation that allergic patients with a high level of allergen-specific IgE show increased expression of eosinophil adhesion molecules and the reported correlation between serum allergen-specific IgE, the number of eosinophils infiltrating the airways and the severity of asthma [8] suggest that FceRII may modulate eosinophil locomotion.…”

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confidence: 99%

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Stimulation of eosinophil IgE low-affinity receptor leads to increased adhesion molecule expression and cell migration

et al. 2000

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Immunoglobulin binding on eosinophil surface receptors results in activation of these cells. Evaluating blood eosinophils from atopic subjects, it was investigated whether ligation of immunoglobulin E low-affinity receptor (FceRII/ CD23) with specific monoclonal antibodies (Mabs) resulted in enhanced eosinophil migration and adhesion molecule expression.Eosinophils from 20 subjects with allergic asthma (atopic individuals) and nine nonatopic normal individuals (controls) were purified using Percoll gradients. The effect of antihuman CD23 Mabs on: 1) eosinophil migration through human umbilical vein endothelial cells (HUVECs); and 2) eosinophil expression of the adhesion molecules leukocyte function-associated antigen-1 (LFA-1, CD11a/CD18), macrophage antigen-1 (Mac-1, CD11b/CD18) and very late activation antigen-1 (VLA-4, CD49d/CD29) was evaluated by specific Mab staining and flow cytometric analysis.As compared to controls, freshly isolated eosinophils from atopic individuals showed enhanced migration through HUVECs (p<0.05) and increased LFA-1 expression (p<0.01), but similar Mac-1 and VLA-4 expression (p>0.1 for both). In both controls and atopic individuals, eosinophil incubation with antihuman CD23 Mabs induced a dose-dependent increase in cell migration through HUVECs, significant at antihuman CD23 Mab concentrations of 5 mg . mL -1 (p>0.05 for all). Similarly, incubation of the cells with antihuman CD23 Mabs induced dose-dependent upregulation of LFA-1 and Mac-1 expression, whereas no changes in VLA-4 expression were observed (p>0.1). Finally, the enhanced eosinophil migration induced by antihuman CD23 Mab stimulation was significantly inhibited by antihuman LFA-1 (84 14% (mean SEM); p<0.01) and VLA-4 Mabs (47 15%; p<0.05) but not by antihuman Mac-1 Mabs (p>0.1).In both atopic and control subjects, immunoglobulin E, low-affinity receptor stimulation induces functional changes in eosinophils characterized by increased eosinophil migration associated with enhanced late function antigen-1 and Mac-1 expression. Eur Respir J 2000; 16: 940±946.

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“…14 On the other hand, it has also been reported that NO donors inhibit the in vitro programmed cell death of human eosinophils, and stimulate the release of TNF-␣ by these important anthelmintic effector cells. 16,17 The cellular sources of the NO derivatives detected in our patients still need to be clarified, especially in the light of the apparent differences in NO generation in comparison with rodents. 18 Two prerequisites, that have been associated with NO production by human monocytes, namely high levels of IFN-␥ and up-regulation of the early activation antigen CD69 on peripheral blood mononuclear cells, have been demonstrated during clearance of microfilaremia in loiasis.…”

mentioning

confidence: 99%

Short report: total serum levels of the nitric oxide derivatives nitrite/nitrate during microfilarial clearance in human filarial disease.

Winkler¹,

Menyawi²,

Linnau³

et al. 1998

The American Journal of Tropical Medicine and Hygiene

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Abstract. Nitric oxide (NO) has recently been shown to be cytotoxic to both microfilariae and adult Brugia malayi in vitro and in a murine model, as well against Onchocerca lienalis microfilariae in vitro. We studied the kinetics of nitrite/nitrate, both stable end products of NO, by high-pressure liquid chromatography during microfilaricidal chemotherapy in four filariasis (three Loa loa, and one Onchocerca volvulus) patients. High serum levels of nitrite/nitrate were released during microfilarial clearance and sustained elevated levels were observed six months after chemotherapy, suggesting a role of NO in the elimination of microfilariae in human filariasis.The microfilaremic state of human filarial infection is associated with a parasite-specific immunologic hyporesponsiveness characterized by an expansion of T helper (Th)-2 cells and a lack of Th-1 cell responses. 1 Microfilaricidal chemotherapy with either diethylcarbamazine (DEC) or ivermectin induces an acute inflammatory reaction accompanied by an interleukin (IL)-5 dependent increase of eosinophils, eosinophil degranulation, and elevated proinflammatory cytokine levels like IL-6, tumor necrosis factor-alpha (TNF-␣) and interferon-gamma (IFN-␥). 2-6 Long-term effects of drug induced microfilarial clearance comprise a reversal of the parasite-specific hyporesponsiveness with restoration of Th-1 cell-mediated responses and resistance to reinfection. [7][8][9] It is therefore assumed that host factors play an essential role in the removal of microfilariae, which is emphasized by the fact that DEC is not microfilaricidal in vitro without host factors, but induces a rapid decrease in microfilarial levels in vivo. 10 Release of toxic granules and reactive oxygen intermediates by activated myeloid cells have all been implicated in microfilarial clearance. 11 However, the precise immune effector mechanisms operating against the developmental stages of filarial disease remain largely unexplored.Nitric oxide (NO) or its by-products have recently been shown to damage microfilariae of Brugia malayi and Onchocerca lienalis in vitro. 12 In addition, inhibitory effects of NO on the development of third-stage (L3) larvae of B. malayi in a murine model and its toxicity on adult B. malayi in vitro have been demonstrated. 13,14 Furthermore, the ivermectin-induced killing of microfilariae of Litosimoides carinii has been shown to be mediated by NO. 15 To determine whether NO plays a role in the removal and the long-term suppression of microfilariae after chemotherapy in human filariasis, serum levels of its stable end products nitrite and nitrate were closely monitored during microfilarial clearance and re-examined six and 12 months after chemotherapy.

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Involvement of FcϵRII/CD23 and L-Arginine Dependent Pathway in IgE-Mediated Activation of Human Eosinophils

Cited by 38 publications

References 0 publications

The Effect of Omalizumab on Eosinophilic Inflammation of the Respiratory Tract in Patients with Allergic Asthma

The Effect of Omalizumab on Eosinophilic Inflammation of the Respiratory Tract in Patients with Allergic Asthma

Stimulation of eosinophil IgE low-affinity receptor leads to increased adhesion molecule expression and cell migration

Short report: total serum levels of the nitric oxide derivatives nitrite/nitrate during microfilarial clearance in human filarial disease.

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