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Published online before print May 18, 2009
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0708452

Received for publication July 31, 2008.
Revised March 9, 2009.
Accepted for publication April 2, 2009.

Article

IL-18 and IL-33 elicit Th2 cytokines from basophils via a MyD88- and p38{alpha}-dependent pathway

Kelly M. Kroeger , Brandon M. Sullivan , and Richard M. Locksley @

Howard Hughes Medical Institute, Departments of Medicine and Microbiology/Immunology, University of California San Francisco, San Francisco, California, USA

@ To whom correspondence should be addressed. E-mail: locksley{at}medicine.ucsf.edu.


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Abstract

IL-4 and IL-13 are instrumental in the development and progression of allergy and atopic disease. Basophils represent a key source of these cytokines and produce IL-4 and IL-13 when stimulated with IL-18, a member of the IL-1 family of cytokines. Comparative analyses of the effects of caspase-1-dependent IL-1 family cytokines on basophil IL-4 and IL-13 production have not been performed, and the signaling pathway proteins required for Fc{varepsilon}RI-independent Th2 cytokine production from basophils remain incompletely defined. Using mouse bone marrow-derived cultured basophils, we found that IL-4 and IL-13 are produced in response to IL-18 or IL-33 stimulation. IL-18- or IL-33-mediated Th2 cytokine production is dependent on MyD88 and p38{alpha} signaling proteins. In addition, basophil survival increased in the presence of IL-18 or IL-33 as a result of increased Akt activation. Studies in vivo confirmed the potency of IL-18 and IL-33 in activating cytokine release from mouse basophils.

Key Words: IL-4 • IL-1 • signaling




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