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IL-23 differentially regulates the Th1/Th17 balance in ulcerative colitis and Crohn's disease
  1. Taku Kobayashi (kobataku{at}z3.keio.jp)
  1. Department of Internal Medicine, Keio University School of Medicine, Japan
    1. Susumu Okamoto (ibdokamo{at}sc.itc.keio.ac.jp)
    1. Department of Internal Medicine, Keio University School of Medicine, Japan
      1. Tadakazu Hisamatsu (hisamachi{at}aol.com)
      1. Department of Internal Medicine, Keio University School of Medicine, Japan
        1. Nobuhiko Kamada (kamanobu{at}excite.co.jp)
        1. Department of Internal Medicine, Keio University School of Medicine, Japan
          1. Hiroshi Chinen (h082483{at}med.u-ryukyu.ac.jp)
          1. Department of Medicine and Therapeutics, University of the Ryukyus, Japan
            1. Riko Saito (ricoichikawa{at}yahoo.co.jp)
            1. Department of Internal Medicine, Keio University School of Medicine, Japan
              1. Mina T Kitazume
              1. Department of Internal Medicine, Keio University School of Medicine, Japan
                1. Atsushi Nakazawa (anakaza{at}aol.com)
                1. Department of Internal Medicine, Keio University School of Medicine, Japan
                  1. Akira Sugita
                  1. Department of Surgery, Yokohama City Hospital, Japan
                    1. Kazutaka Koganei
                    1. Department of Surgery, Yokohama City Hospital, Japan
                      1. Ken-ichi Isobe (kisobe{at}med.nagoya-u.ac.jp)
                      1. Department of Immunology, Nagoya University Graduate Shcool of Medicine, Japan
                        1. Toshifumi Hibi (thibi{at}sc.itc.keio.ac.jp)
                        1. Department of Internal Medicine, Keio University School of Medicine, Japan

                          Abstract

                          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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