IL-18 and IL-33 elicit Th2 cytokines from basophils via a MyD88- and p38alpha-dependent pathway.
J Leukoc Biol
; 86(4): 769-78, 2009 Oct.
Article
em En
| MEDLINE
| ID: mdl-19451398
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 FcepsilonRI-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 p38alpha 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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Basófilos
/
Transdução de Sinais
/
Interleucinas
/
Células Th2
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Interleucina-18
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Proteína Quinase 14 Ativada por Mitógeno
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Fator 88 de Diferenciação Mieloide
Limite:
Animals
Idioma:
En
Revista:
J Leukoc Biol
Ano de publicação:
2009
Tipo de documento:
Article
País de afiliação:
Estados Unidos