Background: A novel Th cell lineage, Th17, that exclusively produces the proinflammatory cytokine interleukin (IL)-17 has been reported to play important roles in various inflammatory diseases. IL-23 is also focused upon for its potential to promote Th17. Here, we investigated the roles of the IL-23/-17 axis in inflammatory bowel diseases such as ulcerative colitis (UC) and Crohn's disease (CD).
Materials and methods: Mucosal samples were obtained from surgically resected specimens (controls: n=12; UC: n=17; CD: n=22). IL-17 production by isolated peripheral blood (PB) and lamina propria (LP) CD4+ cells was examined. Quantitative polymerase chain reaction amplification was performed to determine the mRNA expression levels of IL-17, interferon-gamma (IFN-γ, IL-23 receptor (IL-23R) and retinoic acid-related orphan receptor-gamma (RORC) in LP CD4+ cells, and IL-12 family members, such as IL-12p40, IL-12p35 and IL-23p19, in whole mucosal specimens. The effects of exogenous IL-23 on IL-17 production by LP CD4+ cells were also examined.
Results: IL-17 production was higher in LP CD4+ cells than in PB. Significant IL-17 mRNA upregulation in LP CD4+ cells was found in UC, while IFN-γ was increased in CD. IL-23R and RORC were upregulated in LP CD4+ cells isolated from both UC and CD. IL-17 production was significantly increased by IL-23 in LP CD4+ cells from UC but not CD. Upregulated IL-23p19 mRNA expression was correlated with IL-17 in UC and IFN-γ in CD.
Conclusions: IL-23 may play important roles in controlling the differential Th1/Th17 balance in both UC and CD, although Th17 cells may exist in both diseases.
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