Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 7, Pages 4457-4460Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.7.4457
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Funding
- Department of Pathology, University of Maryland School of Medicine, Baltimore
- National Institutes of Health Grant DK078699 [DK078699]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R21DK078699] Funding Source: NIH RePORTER
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IL-23 has been implicated in the pathogenesis of several tissue-specific autoimmune I 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-1 beta, 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-1 beta alone triggered IL-23 secretion and the IL-IR 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 P-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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