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Human rIL-3 induces histamine release from some human basophils, with cells from atopics responding to a greater extent than non-atopic donors. The dose response curves were highly variable. IL-3 was active on purified basophils and the release process was slower and required more calcium than anti-IgE. Removal of surface IgE from basophils rendered them unresponsive to IL-3. The response could be restored by passive sensitization of basophils with IgE+, IgE known to bind histamine-releasing factors, and not IgE-, IgE unreactive with histamine-releasing factors. Thus, IL-3 uncovers IgE heterogeneity. IL-3 does not, however, directly interact with IgE+. Rather, passive sensitization with IgE+ or stimulation of basophils with low concentrations of several secretagogues renders the cells sensitive to IL-3. IL-3 may well play a pro-inflammatory role by potentiating the effects of IgE+ or various secretagogues.
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September 1989,
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S M MacDonald, and
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S M MacDonald, and
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S M MacDonald, and
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L M Lichtenstein
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S M MacDonald, and
R P Schleimer, and
A Kagey-Sobotka, and
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L M Lichtenstein
September 1991,
Journal of immunology (Baltimore, Md. : 1950),
S M MacDonald, and
R P Schleimer, and
A Kagey-Sobotka, and
S Gillis, and
L M Lichtenstein
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S M MacDonald, and
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L M Lichtenstein
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General pharmacology,
