Cutting edge: IL-1 controls the IL-23 response induced by gliadin, the etiologic agent in celiac disease.
J Immunol
; 181(7): 4457-60, 2008 Oct 01.
Article
em En
| MEDLINE
| ID: mdl-18802048
ABSTRACT
IL-23 has been implicated in the pathogenesis of several tissue-specific autoimmune diseases. Currently, celiac disease (CD) is the only autoimmune disease in which both the major genetic (95% HLA-DQ2(+)) and etiologic factors (dietary glutens) for susceptibility are known. We demonstrate that wheat gliadin induces significantly greater production of IL-23, IL-1beta, and TNF-alpha in PBMC from CD patients compared with HLA-DQ2(+) healthy controls, strongly advocating a role for IL-23 in the pathogenesis of CD. Moreover, IL-1beta alone triggered IL-23 secretion and the IL-1R antagonist inhibited this response in PBMC and purified monocytes. This sequence of events was replicated by beta-glucan, another substance known to induce IL-23 production. Our results suggest that gliadin and beta-glucan stimulate IL-23 secretion through induction of the IL-1 signaling pathway and reveal for the first time that the IL-1 system regulates IL-23 production. These findings may provide therapeutic targets for this disease and other inflammatory conditions mediated by IL-23.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Biossíntese de Proteínas
/
Doença Celíaca
/
Interleucina-1
/
Interleucina-23
/
Gliadina
Tipo de estudo:
Etiology_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2008
Tipo de documento:
Article