Nonreleasing basophils convert to releasing basophils by culturing with IL-3.

The extent of basophil histamine release initiated by IgE cross-linking stimuli has been known to vary greatly among donors. Studies on anti-IgE nonreleasing basophils are useful in understanding the IgE-specific control mechanism of mediator release. We attempted to determine (1) whether a mutation of Fc epsilon RI is present in nonreleasing basophils and (2) whether treatment with IL-3 converts anti-IgE nonreleasing basophils to releasing basophils. Basophils were purified from normal human blood and donors were divided into releasers (maximal histamine release > 5%) and nonreleasers (< 5%). The mutation of Fc epsilon RI alpha, beta, and gamma was evaluated by reverse transcriptase-polymerase chain reaction, and the DNA sequence was determined from amplified polymerase chain reaction products. Although antibodies against Fc epsilon RI failed to cause histamine release in anti-IgE nonreleasing basophils, no primary structural change of Fc epsilon RI was observed in nonreleaser basophils. After culturing with IL-3 for 7 days, nonreleasing basophils released histamine in response to anti-IgE, and dose-response curves of anti-IgE were equal in both releasers and nonreleasers. The conversion of nonreleasing basophils to releasing basophils was evident after 3 days of culture with IL-3. These findings indicate that nonreleasing basophils have recoverable defect(s) in the signal transduction pathway after IgE cross-linking.