Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0708452 on May 18, 2009

Published online before print May 18, 2009
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(Journal of Leukocyte Biology. 2009;86:769-778.)
© 2009 Society for Leukocyte Biology

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. Locksley1

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

1. Correspondence: UCSF, Box 0654, S 1032B, 513 Parnassus Ave., San Francisco, CA 94143-0759, USA. E-mail: locksley{at}medicine.ucsf.edu

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{epsilon}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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