These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: A study of the interrelationship between circulating IgG subclass anti-IgE autoantibodies, IgE and soluble CD23 in asthma.
    Author: Shakib F, Boulstridge L, Smith SJ.
    Journal: Allergol Immunopathol (Madr); 1993; 21(1):20-4. PubMed ID: 7687088.
    Abstract:
    In this paper we hypothesise that circulating autoanti-IgE antibodies, which are found in allergic asthma patients, could potentially enhance IgE synthesis by blocking its binding to CD23 on B lymphocytes, thereby potentiating the release of soluble fragments of CD23 which have B cell growth-promoting activity. We have investigated this possibility indirectly by measuring soluble (s) CD23 and IgG subclass anti-IgE antibody levels in asthmatic patients' sera, to find out if the two parameters are related. However, we were unable to show any significant correlations between serum IgG subclass anti-IgE activities and sCD23 levels. This may have been due, at least in part, to the heterogeneous epitope specificity of the autoanti-IgE being detected. Interestingly, there was a significant inverse correlation (p = 0.0178) between serum IgE and sCD23 levels in asthma; an observation which underlines the notion that binding of IgE to membrane CD23 abrogates the release of sCD23. The present study confirms and extends previous reports of significantly raised circulating levels of IgG anti-IgE in asthma patients (p = 0.0004), by further demonstrating that IgG anti-IgE is mostly restricted to IgG1. Given that IgG1 binds very efficiently to C1q and Fc gamma Rs, our observation lends further support to the notion that IgG anti-IgE may facilitate the removal of IgE-allergen complexes by triggering IgG effector function pathways.
    [Abstract] [Full Text] [Related] [New Search]