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Characterization of human T cell-derived IgE-potentiating factor
European Journal of Immunology
|August 1, 1986
Summary
Researchers found that IgE-potentiating factors from Fc epsilon receptor-positive (Fc epsilon R+) T cells selectively enhance IgE synthesis in atopic B cells. These factors target specific B cells and share characteristics with rodent IgE-potentiating factors.
Area of Science:
- Immunology
- Allergy Research
- Molecular Biology
Background:
- Previous studies demonstrated Fc epsilon receptor-positive (Fc epsilon R+) T cell lines from hyper IgE syndrome patients secrete IgE-binding factors.
- These factors selectively enhance immunoglobulin E (IgE) but not immunoglobulin G (IgG) synthesis in B cells from allergic rhinitis patients, not nonatopic subjects.
Purpose of the Study:
- To investigate the effect of supernatants from Fc epsilon R+ T cell lines on a panel of B cells from atopic patients.
- To further characterize the IgE-potentiating factors derived from Fc epsilon R+ T cell lines.
Main Methods:
- Testing supernatants from Fc epsilon R+ T cell lines on B cells from 20 atopic patients.
- Characterizing IgE-potentiating factors using Sephadex G-75 fractionation and lectin affinity.
- Assessing the impact of exogenous human IgE and tunicamycin on factor release.
Main Results:
- IgE synthesis was selectively enhanced only in atopic B cell cultures with ongoing spontaneous IgE synthesis.
- The target of IgE-potentiating factors was identified as large, low-density B cells in atopic donors.
- Factors fractionated into two peaks (15,000 and 60,000 kDa) with affinity for lentil lectin but not peanut agglutinin.
- Factor release was enhanced by exogenous human IgE and inhibited by tunicamycin (an N-glycosylation inhibitor).
Conclusions:
- Human IgE-potentiating factors selectively enhance IgE synthesis in specific atopic B cells.
- Physicochemical characteristics of human IgE-potentiating factors show homology with rodent factors.
- These findings highlight the complex immune regulation of IgE production in atopy.