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Updated: Oct 19, 2026

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity
Published on: September 16, 2011
Augmentation of antigen-stimulated histamine release from human basophils by serum-treated zymosan particles. II.
It was observed previously that serum-treated zymosan particles (Zx) augmented antigen and anti-IgE stimulated histamine release. With most of the enhancement attributed to an increased rate of release, this suggested that Zx was active only during the course of IgE-mediated release. This association between IgE-mediated histamine release and responsiveness to Zx was examined further in the present report. Addition of Zx at various time intervals after release had been initiated indicated that the basophil responsiveness to Zx was limited in duration; maximum responsiveness to Zx correlated closely with the period in which the rate of IgE-mediated histamine release was maximum. The time-dependent decline in sensitivity to Zx paralleled the kinetics for desensitization to antigen. Addition of Zx failed to cause release from basophils desensitized in vitro or from basophils of a donor who failed to release histamine upon challenge with anti-IgE. In contrast to the enhancement of IgE-mediated release, Zx did not augment histamine release caused by C5a or the synthetic peptide f-Met-Leu-Phe. It is concluded that an obligatory link exists between ongoing IgE-mediated histamine release and enhancement by Zx.
It was observed previously that serum-treated zymosan particles (Zx) augmented antigen and anti-IgE stimulated histamine release. With most of the enhancement attributed to an increased rate of release, this suggested that Zx was active only during the course of IgE-mediated release. This association between IgE-mediated histamine release and responsiveness to Zx was examined further in the present report. Addition of Zx at various time intervals after release had been initiated indicated that the basophil responsiveness to Zx was limited in duration; maximum responsiveness to Zx correlated closely with the period in which the rate of IgE-mediated histamine release was maximum. The time-dependent decline in sensitivity to Zx paralleled the kinetics for desensitization to antigen. Addition of Zx failed to cause release from basophils desensitized in vitro or from basophils of a donor who failed to release histamine upon challenge with anti-IgE. In contrast to the enhancement of IgE-mediated release, Zx did not augment histamine release caused by C5a or the synthetic peptide f-Met-Leu-Phe. It is concluded that an obligatory link exists between ongoing IgE-mediated histamine release and enhancement by Zx.
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