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The relationship between serum IgE and surface levels of FcϵR on human leukocytes in various diseases: Correlation of expression with FcϵRI on basophils but not on monocytes or eosinophils

Background: Expression of receptors for IgE (FcϵR) have been mainly studied on mast cells and blood basophils in the context of allergic disease. Some reports have noted limited expression of FcϵR on other leukocytes, including blood monocytes and eosinophils in certain patients. An association betw...

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Published in:Journal of allergy and clinical immunology 2000-09, Vol.106 (3), p.514-520
Main Authors: Saini, Sarbjit S., Klion, Amy D., Holland, Steven M., Hamilton, Robert G., Bochner, Bruce S., MacGlashan, Donald W.
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container_title Journal of allergy and clinical immunology
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Klion, Amy D.
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Bochner, Bruce S.
MacGlashan, Donald W.
description Background: Expression of receptors for IgE (FcϵR) have been mainly studied on mast cells and blood basophils in the context of allergic disease. Some reports have noted limited expression of FcϵR on other leukocytes, including blood monocytes and eosinophils in certain patients. An association between human blood basophil expression of FcϵRIα and serum IgE has been noted among allergic subjects. Objective: Recent evidence supports regulation of FcϵRIα by free IgE on both mast cells and basophils. We hypothesized that this relationship would exist across an extremely wide range of IgE levels for human basophils, irrespective of underlying disease. We further examined whether a similar relationship existed between serum IgE and FcϵRIα or FcϵRII (CD23) expression on monocytes and eosinophils in these same subjects. Methods: Blood was obtained from nonallergic subjects (n = 3) and subjects with allergic asthma (n = 5), atopic dermatitis (n = 3), hypereosinophilic syndromes (n = 7), hyper-IgE syndrome (n = 6), helminth infestation (n = 6), or IgE myeloma (n = 1). Levels of serum IgE were determined by using RIA and ranged from 3 to 4.7 mg/mL. Levels of cell surface FcϵRIα, FcϵRII, and IgE were measured by using immunofluorescence and flow cytometry. Results: Basophil surface IgE density and FcϵRIα expression correlated with serum IgE levels (r = 0.67 and r = 0.46, respectively; P < .01; n = 31) regardless of the disease state. In contrast, monocyte FcϵRIα expression did not correlate with serum IgE (r = 0.09, P > .5, n = 29), and low-level eosinophil FcϵRIα expression was only detected in a single asthmatic subject. CD23 expression was not detected on basophils or eosinophils, except for the eosinophils from the donor with IgE myeloma. CD23 was present on monocytes from some donors but did not correlate with serum IgE levels. Conclusions: In a variety of disease states, FcϵRIα expression by basophils, but not monocytes or eosinophils, correlated with serum IgE levels across a 6-log range of IgE. These data support the concept of in vivo regulation of FcϵRIα on basophils by serum IgE and further demonstrate that this is independent of allergic disease per se. (J Allergy Clin Immunol 2000;106:514-20.)
doi_str_mv 10.1067/mai.2000.108431
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Some reports have noted limited expression of FcϵR on other leukocytes, including blood monocytes and eosinophils in certain patients. An association between human blood basophil expression of FcϵRIα and serum IgE has been noted among allergic subjects. Objective: Recent evidence supports regulation of FcϵRIα by free IgE on both mast cells and basophils. We hypothesized that this relationship would exist across an extremely wide range of IgE levels for human basophils, irrespective of underlying disease. We further examined whether a similar relationship existed between serum IgE and FcϵRIα or FcϵRII (CD23) expression on monocytes and eosinophils in these same subjects. Methods: Blood was obtained from nonallergic subjects (n = 3) and subjects with allergic asthma (n = 5), atopic dermatitis (n = 3), hypereosinophilic syndromes (n = 7), hyper-IgE syndrome (n = 6), helminth infestation (n = 6), or IgE myeloma (n = 1). Levels of serum IgE were determined by using RIA and ranged from 3 to 4.7 mg/mL. Levels of cell surface FcϵRIα, FcϵRII, and IgE were measured by using immunofluorescence and flow cytometry. Results: Basophil surface IgE density and FcϵRIα expression correlated with serum IgE levels (r = 0.67 and r = 0.46, respectively; P &lt; .01; n = 31) regardless of the disease state. In contrast, monocyte FcϵRIα expression did not correlate with serum IgE (r = 0.09, P &gt; .5, n = 29), and low-level eosinophil FcϵRIα expression was only detected in a single asthmatic subject. CD23 expression was not detected on basophils or eosinophils, except for the eosinophils from the donor with IgE myeloma. CD23 was present on monocytes from some donors but did not correlate with serum IgE levels. Conclusions: In a variety of disease states, FcϵRIα expression by basophils, but not monocytes or eosinophils, correlated with serum IgE levels across a 6-log range of IgE. These data support the concept of in vivo regulation of FcϵRIα on basophils by serum IgE and further demonstrate that this is independent of allergic disease per se. 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Some reports have noted limited expression of FcϵR on other leukocytes, including blood monocytes and eosinophils in certain patients. An association between human blood basophil expression of FcϵRIα and serum IgE has been noted among allergic subjects. Objective: Recent evidence supports regulation of FcϵRIα by free IgE on both mast cells and basophils. We hypothesized that this relationship would exist across an extremely wide range of IgE levels for human basophils, irrespective of underlying disease. We further examined whether a similar relationship existed between serum IgE and FcϵRIα or FcϵRII (CD23) expression on monocytes and eosinophils in these same subjects. Methods: Blood was obtained from nonallergic subjects (n = 3) and subjects with allergic asthma (n = 5), atopic dermatitis (n = 3), hypereosinophilic syndromes (n = 7), hyper-IgE syndrome (n = 6), helminth infestation (n = 6), or IgE myeloma (n = 1). Levels of serum IgE were determined by using RIA and ranged from 3 to 4.7 mg/mL. Levels of cell surface FcϵRIα, FcϵRII, and IgE were measured by using immunofluorescence and flow cytometry. Results: Basophil surface IgE density and FcϵRIα expression correlated with serum IgE levels (r = 0.67 and r = 0.46, respectively; P &lt; .01; n = 31) regardless of the disease state. In contrast, monocyte FcϵRIα expression did not correlate with serum IgE (r = 0.09, P &gt; .5, n = 29), and low-level eosinophil FcϵRIα expression was only detected in a single asthmatic subject. CD23 expression was not detected on basophils or eosinophils, except for the eosinophils from the donor with IgE myeloma. CD23 was present on monocytes from some donors but did not correlate with serum IgE levels. Conclusions: In a variety of disease states, FcϵRIα expression by basophils, but not monocytes or eosinophils, correlated with serum IgE levels across a 6-log range of IgE. These data support the concept of in vivo regulation of FcϵRIα on basophils by serum IgE and further demonstrate that this is independent of allergic disease per se. 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Some reports have noted limited expression of FcϵR on other leukocytes, including blood monocytes and eosinophils in certain patients. An association between human blood basophil expression of FcϵRIα and serum IgE has been noted among allergic subjects. Objective: Recent evidence supports regulation of FcϵRIα by free IgE on both mast cells and basophils. We hypothesized that this relationship would exist across an extremely wide range of IgE levels for human basophils, irrespective of underlying disease. We further examined whether a similar relationship existed between serum IgE and FcϵRIα or FcϵRII (CD23) expression on monocytes and eosinophils in these same subjects. Methods: Blood was obtained from nonallergic subjects (n = 3) and subjects with allergic asthma (n = 5), atopic dermatitis (n = 3), hypereosinophilic syndromes (n = 7), hyper-IgE syndrome (n = 6), helminth infestation (n = 6), or IgE myeloma (n = 1). Levels of serum IgE were determined by using RIA and ranged from 3 to 4.7 mg/mL. Levels of cell surface FcϵRIα, FcϵRII, and IgE were measured by using immunofluorescence and flow cytometry. Results: Basophil surface IgE density and FcϵRIα expression correlated with serum IgE levels (r = 0.67 and r = 0.46, respectively; P &lt; .01; n = 31) regardless of the disease state. In contrast, monocyte FcϵRIα expression did not correlate with serum IgE (r = 0.09, P &gt; .5, n = 29), and low-level eosinophil FcϵRIα expression was only detected in a single asthmatic subject. CD23 expression was not detected on basophils or eosinophils, except for the eosinophils from the donor with IgE myeloma. CD23 was present on monocytes from some donors but did not correlate with serum IgE levels. Conclusions: In a variety of disease states, FcϵRIα expression by basophils, but not monocytes or eosinophils, correlated with serum IgE levels across a 6-log range of IgE. 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subjects AFc receptors
Allergic diseases
basophils
Biological and medical sciences
eosinophils
General aspects
IgE antibody
IgE receptors
Immunopathology
Medical sciences
monocytes
title The relationship between serum IgE and surface levels of FcϵR on human leukocytes in various diseases: Correlation of expression with FcϵRI on basophils but not on monocytes or eosinophils
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