The monocyte/IgE connection: May polymorphisms in the CD14 gene teach us about IgE regulation?

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Abstract

Background: Total IgE levels are known to be under genetic control. Linkage studies have indicated that one or more loci on chromosome 5q may control total IgE, as well as asthma and bronchial hyperresponsiveness to nonspecific stimuli. Our group has undertaken a systematic analysis of chromosome 5q, and has recently characterized five single nucleotide polymorphisms at position -1619, -1359, -1145, -809 and -159 in the promoter of the gene encoding CD14, the myeloid pattern recognition receptor that is critical for efficient innate immune response to lipopolysaccharide (LPS) and bacterial ligands. Methods: Carriers of the major CD14 haplotypes were analyzed for serum levels of IgE and soluble CD14. In vitro IgE synthesis was assessed in peripheral blood mononuclear cells stimulated with IL-4 in the presence or absence of LPS or anti-CD14 monoclonal antibodies. Results: An inverse correlation was found between serum levels of IgE and soluble CD14. On the other hand, in vitro IL-4-dependent IgE synthesis was strongly upregulated by LPS, but suppressed by anti-CD14 monoclonal antibodies. Conclusions: Our results highlight the complex role played by monocytes in IgE regulation.

Original languageEnglish (US)
Pages (from-to)20-24
Number of pages5
JournalInternational Archives of Allergy and Immunology
Volume124
Issue number1-3
DOIs
StatePublished - 2001

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Immunoglobulin E
Monocytes
Genes
Lipopolysaccharides
Interleukin-4
Chromosomes
Monoclonal Antibodies
Pattern Recognition Receptors
Serum
Innate Immunity
Haplotypes
Single Nucleotide Polymorphism
Blood Cells
Asthma
Ligands

Keywords

  • CD14
  • IgE
  • IL-4
  • Monocytes
  • Polymorphism, genetic

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

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title = "The monocyte/IgE connection: May polymorphisms in the CD14 gene teach us about IgE regulation?",
abstract = "Background: Total IgE levels are known to be under genetic control. Linkage studies have indicated that one or more loci on chromosome 5q may control total IgE, as well as asthma and bronchial hyperresponsiveness to nonspecific stimuli. Our group has undertaken a systematic analysis of chromosome 5q, and has recently characterized five single nucleotide polymorphisms at position -1619, -1359, -1145, -809 and -159 in the promoter of the gene encoding CD14, the myeloid pattern recognition receptor that is critical for efficient innate immune response to lipopolysaccharide (LPS) and bacterial ligands. Methods: Carriers of the major CD14 haplotypes were analyzed for serum levels of IgE and soluble CD14. In vitro IgE synthesis was assessed in peripheral blood mononuclear cells stimulated with IL-4 in the presence or absence of LPS or anti-CD14 monoclonal antibodies. Results: An inverse correlation was found between serum levels of IgE and soluble CD14. On the other hand, in vitro IL-4-dependent IgE synthesis was strongly upregulated by LPS, but suppressed by anti-CD14 monoclonal antibodies. Conclusions: Our results highlight the complex role played by monocytes in IgE regulation.",
keywords = "CD14, IgE, IL-4, Monocytes, Polymorphism, genetic",
author = "Donata Vercelli and Mauro Baldini and Fernando Martinez",
year = "2001",
doi = "10.1159/000053658",
language = "English (US)",
volume = "124",
pages = "20--24",
journal = "International Archives of Allergy and Immunology",
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number = "1-3",

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T1 - The monocyte/IgE connection

T2 - May polymorphisms in the CD14 gene teach us about IgE regulation?

AU - Vercelli, Donata

AU - Baldini, Mauro

AU - Martinez, Fernando

PY - 2001

Y1 - 2001

N2 - Background: Total IgE levels are known to be under genetic control. Linkage studies have indicated that one or more loci on chromosome 5q may control total IgE, as well as asthma and bronchial hyperresponsiveness to nonspecific stimuli. Our group has undertaken a systematic analysis of chromosome 5q, and has recently characterized five single nucleotide polymorphisms at position -1619, -1359, -1145, -809 and -159 in the promoter of the gene encoding CD14, the myeloid pattern recognition receptor that is critical for efficient innate immune response to lipopolysaccharide (LPS) and bacterial ligands. Methods: Carriers of the major CD14 haplotypes were analyzed for serum levels of IgE and soluble CD14. In vitro IgE synthesis was assessed in peripheral blood mononuclear cells stimulated with IL-4 in the presence or absence of LPS or anti-CD14 monoclonal antibodies. Results: An inverse correlation was found between serum levels of IgE and soluble CD14. On the other hand, in vitro IL-4-dependent IgE synthesis was strongly upregulated by LPS, but suppressed by anti-CD14 monoclonal antibodies. Conclusions: Our results highlight the complex role played by monocytes in IgE regulation.

AB - Background: Total IgE levels are known to be under genetic control. Linkage studies have indicated that one or more loci on chromosome 5q may control total IgE, as well as asthma and bronchial hyperresponsiveness to nonspecific stimuli. Our group has undertaken a systematic analysis of chromosome 5q, and has recently characterized five single nucleotide polymorphisms at position -1619, -1359, -1145, -809 and -159 in the promoter of the gene encoding CD14, the myeloid pattern recognition receptor that is critical for efficient innate immune response to lipopolysaccharide (LPS) and bacterial ligands. Methods: Carriers of the major CD14 haplotypes were analyzed for serum levels of IgE and soluble CD14. In vitro IgE synthesis was assessed in peripheral blood mononuclear cells stimulated with IL-4 in the presence or absence of LPS or anti-CD14 monoclonal antibodies. Results: An inverse correlation was found between serum levels of IgE and soluble CD14. On the other hand, in vitro IL-4-dependent IgE synthesis was strongly upregulated by LPS, but suppressed by anti-CD14 monoclonal antibodies. Conclusions: Our results highlight the complex role played by monocytes in IgE regulation.

KW - CD14

KW - IgE

KW - IL-4

KW - Monocytes

KW - Polymorphism, genetic

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