IL-18 and IL-33 elicit Th2 cytokines from basophils via a MyD88-and p38α-dependent pathway

被引：130
作者：
Kroeger, Kelly M. [1 ]
Sullivan, Brandon M. [1 ]
Locksley, Richard M. [1 ]
机构：
[1] Univ Calif San Francisco, Dept Med Microbiol & Immunol, Howard Hughes Med Inst, San Francisco, CA 94143 USA
来源：
JOURNAL OF LEUKOCYTE BIOLOGY | 2009年 / 86卷 / 04期
基金：
美国国家卫生研究院;
关键词：
IL-4; IL-1; signaling; ACTIVATED PROTEIN-KINASE; ALLERGIC AIRWAY INFLAMMATION; SIGNAL-TRANSDUCTION PATHWAYS; IFN-GAMMA PRODUCTION; N-TERMINAL KINASE; HUMAN MAST-CELLS; BLOOD BASOPHILS; SERINE PHOSPHORYLATION; RECEPTOR FAMILY; TYPE-2; IMMUNITY;
D O I：
10.1189/jlb.0708452
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
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. J. Leukoc. Biol. 86: 769-778; 2009.
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收藏
页码：769 / 778
页数：10
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