Literature DB >> 18512248

IL-23/IL-17 immunity as a hallmark of Crohn's disease.

Veera Hölttä1, Paula Klemetti, Taina Sipponen, Mia Westerholm-Ormio, Guillermo Kociubinski, Harri Salo, Laura Räsänen, Kaija-Leena Kolho, Martti Färkkilä, Erkki Savilahti, Outi Vaarala.   

Abstract

BACKGROUND: We studied the balance between ileal T-effector cells versus T-regulatory cells in active and inactive Crohn's disease (CD).
METHODS: We compared effector and regulatory T-cell-related markers such as interleukin (IL)-17, interferon (IFN)-gamma, IL-4, and Foxp3 transforming growth factor (TGF)-beta CTLA-4 and markers for innate immune activation such as IL-6, IL-10, IL-18, IL-23, tumor necrosis factor (TNF)-alpha, and IL-12p70, studied with immunohistochemistry and RT-PCR in ileal biopsies from patients with active or inactive CD and from control subjects. IL-17 in fecal samples was detected by ELISA. The effect of IL-17 on IL-8 and TNF-alpha mRNA expression in epithelial cell line Caco-2 was studied.
RESULTS: The numbers of IL-4-, IL-17-, and IL-23(p19)-positive cells in the lamina propria were higher in patients with CD, both active and inactive, than in the controls. mRNA expression of IL-17A, IL-6, and Foxp3 was increased in the biopsies both from patients with active disease and those in remission, whereas mRNA expression of IL-23 was increased only in active disease. Fecal IL-17 concentration was increased in patients with active disease. IL-17 enhanced the IL-8 and TNF-alpha response of the epithelial cell line to lipopolysaccharide (LPS) in vitro.
CONCLUSIONS: Our findings suggest that activation of the IL-23/IL-17 axis is fundamentally connected to the etiology of CD and may represent the basis for the relapsing nature of the disease by increasing the sensitivity of epithelium to microbial LPS.

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Year:  2008        PMID: 18512248     DOI: 10.1002/ibd.20475

Source DB:  PubMed          Journal:  Inflamm Bowel Dis        ISSN: 1078-0998            Impact factor:   5.325


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