Human recombinant granulocyte-macrophage colony-stimulating factor and interleukin 3 cause basophil histamine release.

M Haak-Frendscho; N Arai; K Arai; M L Baeza; A Finn; A P Kaplan

doi:10.1172/JCI113567

Division of Allergy, Rheumatology, and Clinical Immunology, State University of New York, Stony Brook 11798-8161.

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Division of Allergy, Rheumatology, and Clinical Immunology, State University of New York, Stony Brook 11798-8161.

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Division of Allergy, Rheumatology, and Clinical Immunology, State University of New York, Stony Brook 11798-8161.

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Division of Allergy, Rheumatology, and Clinical Immunology, State University of New York, Stony Brook 11798-8161.

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Division of Allergy, Rheumatology, and Clinical Immunology, State University of New York, Stony Brook 11798-8161.

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Division of Allergy, Rheumatology, and Clinical Immunology, State University of New York, Stony Brook 11798-8161.

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Published in Volume 82, Issue 1 on July 1, 1988
J Clin Invest. 1988;82(1):17–20. https://doi.org/10.1172/JCI113567.
© 1988 The American Society for Clinical Investigation

Published July 1, 1988 - Version history

Histamine-releasing factors (HRFs) have been shown to be released from a variety of human cells, including T lymphocytes and alveolar macrophages. We considered the possibility that known cytokines might possess such activity on human basophils and/or mast cells and therefore tested preparations of human recombinant IL 3, IL 4, IL 5, granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) upon a panel of basophil donors. IL 3 and GM-CSF possessed significant histamine-releasing activity in 8 of 10 and 12 of 14 subjects, respectively. In each instance, a dose response could be demonstrated. IL 4 and G-CSF had no such activity, whereas IL 5 had activity in only 2 of 14 donors tested. We conclude that IL 3 and GM-CSF represent two effective HRFs, and suggest that HRF, as isolated based upon histamine-releasing activity, is likely to be heterogeneous in terms of molecular identity. Whether previously described HRFs relate specifically to IL 3 or GM-CSF must await primary sequence analysis of HRF and/or studies with monospecific antisera.

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