The IgE system

Donata Vercelli, R. S. Geha

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The data presented herein indicate that IgE synthesis results from a complex interaction between T cells, B cells, and monocytes, under the control of T cell-derived and monocyte-derived lymphokines (IL-4, IL-5, and IL-6). In addition to their direct effects on IgE synthesis, these lymphokines have other functions, many of which are related to IgE. IL-4 is not only a crucial signal for the induction of IgE synthesis, but also a growth factor for murine mast cells together with IL-3, a product of the same T cell clones. Furthermore, IL-4 is a potent inducer of FcεR2b expression on both B cells and monocytes. On the other hand, IL-4-secreting T cells also produce IL-5, which promotes B cell maturation and induces differentiation of eosinophil precursors. Eosinophils, in turn, express CD23 when activated; thus, the activation of the IgE system leads to increased IgE synthesis and to enhanced expression of FcεR1 (on mast cells) and FcεR2 (on B cells, monocytes, and eosinophils). This in turn results in increased receptor-ligand interactions, with release of different chemical mediators involved in the pathogenesis of allergy. Such considerations suggest that the regulation of IgE synthesis should be viewed in the wider context of the IgE system, a multi-component network in which different cell types are functionally integrated mainly through lymphokine-mediated signals. A comprehensive view of the IgE system can provide an explanation for several frequent clinical observations, eg, the association between increased IgE production and eosinophilia in a number of diseases - including allergic and parasitic disease, acute graft-versus-host disease, and some immunodeficiency diseases - and the presence of increased numbers of circulating CD23+ monocytes in atopic patients. Furthermore, this approach may lead to the development of more effective strategies for the treatment of allergy.

Original languageEnglish (US)
Pages (from-to)4-11
Number of pages8
JournalAnnals of Allergy
Volume63
Issue number1
StatePublished - 1989
Externally publishedYes

Fingerprint

Immunoglobulin E
Monocytes
Interleukin-4
Lymphokines
B-Lymphocytes
Eosinophils
T-Lymphocytes
Interleukin-5
Hypersensitivity
Parasitic Diseases
Stem Cell Factor
Interleukin-3
Eosinophilia
Graft vs Host Disease
Mast Cells
Interleukin-6
Clone Cells
Ligands

ASJC Scopus subject areas

  • Immunology and Allergy

Cite this

Vercelli, D., & Geha, R. S. (1989). The IgE system. Annals of Allergy, 63(1), 4-11.

The IgE system. / Vercelli, Donata; Geha, R. S.

In: Annals of Allergy, Vol. 63, No. 1, 1989, p. 4-11.

Research output: Contribution to journalArticle

Vercelli, D & Geha, RS 1989, 'The IgE system', Annals of Allergy, vol. 63, no. 1, pp. 4-11.
Vercelli D, Geha RS. The IgE system. Annals of Allergy. 1989;63(1):4-11.
Vercelli, Donata ; Geha, R. S. / The IgE system. In: Annals of Allergy. 1989 ; Vol. 63, No. 1. pp. 4-11.
@article{81e1b4c542af45eab7603fee0c698e03,
title = "The IgE system",
abstract = "The data presented herein indicate that IgE synthesis results from a complex interaction between T cells, B cells, and monocytes, under the control of T cell-derived and monocyte-derived lymphokines (IL-4, IL-5, and IL-6). In addition to their direct effects on IgE synthesis, these lymphokines have other functions, many of which are related to IgE. IL-4 is not only a crucial signal for the induction of IgE synthesis, but also a growth factor for murine mast cells together with IL-3, a product of the same T cell clones. Furthermore, IL-4 is a potent inducer of FcεR2b expression on both B cells and monocytes. On the other hand, IL-4-secreting T cells also produce IL-5, which promotes B cell maturation and induces differentiation of eosinophil precursors. Eosinophils, in turn, express CD23 when activated; thus, the activation of the IgE system leads to increased IgE synthesis and to enhanced expression of FcεR1 (on mast cells) and FcεR2 (on B cells, monocytes, and eosinophils). This in turn results in increased receptor-ligand interactions, with release of different chemical mediators involved in the pathogenesis of allergy. Such considerations suggest that the regulation of IgE synthesis should be viewed in the wider context of the IgE system, a multi-component network in which different cell types are functionally integrated mainly through lymphokine-mediated signals. A comprehensive view of the IgE system can provide an explanation for several frequent clinical observations, eg, the association between increased IgE production and eosinophilia in a number of diseases - including allergic and parasitic disease, acute graft-versus-host disease, and some immunodeficiency diseases - and the presence of increased numbers of circulating CD23+ monocytes in atopic patients. Furthermore, this approach may lead to the development of more effective strategies for the treatment of allergy.",
author = "Donata Vercelli and Geha, {R. S.}",
year = "1989",
language = "English (US)",
volume = "63",
pages = "4--11",
journal = "Annals of Allergy, Asthma and Immunology",
issn = "1081-1206",
publisher = "American College of Allergy, Asthma and Immunology",
number = "1",

}

TY - JOUR

T1 - The IgE system

AU - Vercelli, Donata

AU - Geha, R. S.

PY - 1989

Y1 - 1989

N2 - The data presented herein indicate that IgE synthesis results from a complex interaction between T cells, B cells, and monocytes, under the control of T cell-derived and monocyte-derived lymphokines (IL-4, IL-5, and IL-6). In addition to their direct effects on IgE synthesis, these lymphokines have other functions, many of which are related to IgE. IL-4 is not only a crucial signal for the induction of IgE synthesis, but also a growth factor for murine mast cells together with IL-3, a product of the same T cell clones. Furthermore, IL-4 is a potent inducer of FcεR2b expression on both B cells and monocytes. On the other hand, IL-4-secreting T cells also produce IL-5, which promotes B cell maturation and induces differentiation of eosinophil precursors. Eosinophils, in turn, express CD23 when activated; thus, the activation of the IgE system leads to increased IgE synthesis and to enhanced expression of FcεR1 (on mast cells) and FcεR2 (on B cells, monocytes, and eosinophils). This in turn results in increased receptor-ligand interactions, with release of different chemical mediators involved in the pathogenesis of allergy. Such considerations suggest that the regulation of IgE synthesis should be viewed in the wider context of the IgE system, a multi-component network in which different cell types are functionally integrated mainly through lymphokine-mediated signals. A comprehensive view of the IgE system can provide an explanation for several frequent clinical observations, eg, the association between increased IgE production and eosinophilia in a number of diseases - including allergic and parasitic disease, acute graft-versus-host disease, and some immunodeficiency diseases - and the presence of increased numbers of circulating CD23+ monocytes in atopic patients. Furthermore, this approach may lead to the development of more effective strategies for the treatment of allergy.

AB - The data presented herein indicate that IgE synthesis results from a complex interaction between T cells, B cells, and monocytes, under the control of T cell-derived and monocyte-derived lymphokines (IL-4, IL-5, and IL-6). In addition to their direct effects on IgE synthesis, these lymphokines have other functions, many of which are related to IgE. IL-4 is not only a crucial signal for the induction of IgE synthesis, but also a growth factor for murine mast cells together with IL-3, a product of the same T cell clones. Furthermore, IL-4 is a potent inducer of FcεR2b expression on both B cells and monocytes. On the other hand, IL-4-secreting T cells also produce IL-5, which promotes B cell maturation and induces differentiation of eosinophil precursors. Eosinophils, in turn, express CD23 when activated; thus, the activation of the IgE system leads to increased IgE synthesis and to enhanced expression of FcεR1 (on mast cells) and FcεR2 (on B cells, monocytes, and eosinophils). This in turn results in increased receptor-ligand interactions, with release of different chemical mediators involved in the pathogenesis of allergy. Such considerations suggest that the regulation of IgE synthesis should be viewed in the wider context of the IgE system, a multi-component network in which different cell types are functionally integrated mainly through lymphokine-mediated signals. A comprehensive view of the IgE system can provide an explanation for several frequent clinical observations, eg, the association between increased IgE production and eosinophilia in a number of diseases - including allergic and parasitic disease, acute graft-versus-host disease, and some immunodeficiency diseases - and the presence of increased numbers of circulating CD23+ monocytes in atopic patients. Furthermore, this approach may lead to the development of more effective strategies for the treatment of allergy.

UR - http://www.scopus.com/inward/record.url?scp=0024374801&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024374801&partnerID=8YFLogxK

M3 - Article

C2 - 2525888

AN - SCOPUS:0024374801

VL - 63

SP - 4

EP - 11

JO - Annals of Allergy, Asthma and Immunology

JF - Annals of Allergy, Asthma and Immunology

SN - 1081-1206

IS - 1

ER -