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

Abstract

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.

A comprehensive association study for genes in inflammation pathway provides support for their roles in prostate cancer risk in the CAPS study

“…It was found to be involved in the differentiation and survival of various cell types in the peripheral and central nervous systems [16]. FCER2 encodes the low affinity receptor for IgE (FceRII), which is mainly expressed by B cells, monocytes, and eosinophils, and upregulated by IL-4 and IL-13 [17][18][19]. On B cells, FceRII regulates production of IgE and on eosinophils promotes migration and adhesion, suggesting its importance in atopic disease.…”

Fluticasone Propionate Downregulates Nasal Fibroblast Functions Involved in Airway Inflammation and Remodeling

“…In addition to adhesion molecule expression, recruitment of eosinophils in the target tissue requires chemotactic signals released by activated inflammatory cells [36]. Nasal polyp tissue-derived fibroblasts may effectively release high amounts of chemotactic factors for eosinophils, such as eotaxin [10], which specifically attracts this type of cells.…”

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

“…Capron et al [83] observed that the use of anti-CD23 mAb can inhibit IgE-dependent cytotoxicity of eosinophils. 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.…”