Syk deficiency in non-releaser basophils

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Christopher Kepley, Associate Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
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Abstract: Background: Peripheral blood basophils from 10% to 20% of donors fail to degranulate in response to cross-linking the high-affinity IgE receptor FceRI. The molecular mechanisms underlying the nonreleaser phenotype have not been established. Objectives: Our aim was to compare the expression of FceRI-associated protein tyrosine kinases between nonreleaser and releaser basophils. Methods: With use of Western blotting we investigated Syk and Lyn protein levels in highly purified basophils from 3 anti-IgE nonreleasers and 2 releasers. Results: We identified 3 healthy nonatopic donors whose nonreleaser basophils express FceRI normally but fail to express protein for the tyrosine kinase Syk, which is implicated in the initiation of FceRI-mediated secretion. Protein levels for the tyrosine kinase Lyn are somewhat reduced but not absent in nonreleaser basophils. Levels of Lyn and Syk protein are similar in B cells, eosinophils, and neutrophilsfrom releaser and nonreleaser donors. During these studies one nonreleaser “converted” into a releaser with concomitant basophil Syk expression. Conclusion: The absence of detectable Syk could explain the nonreleaser phenotype of basophils from some donors.

Additional Information

Journal of Allergy and Clinical Immunology 1999; 104:279-84.
Language: English
Date: 1999
Basophils, signal transduction, nonreleaser, tyrosine kinase, Lyn, Syk, human

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