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Otuka, A., Nakajima, A., Kubo, M., Wgawa, G., Honda, T., Kitoh, A., Nomura, T., Hanakawa, S., SagitaMoniaga, C., Kim, B., Matsuoka, S., Watanabe, T., Miyachi, Y. and Kabashima, K. (2013) Basophils Are Required for the Induction of Th2 Immunity to Haptens and Peptide Antigens. Nature Communications, 4, Article No. 1738.

has been cited by the following article:

• TITLE: Atopic Dermatitis Deteriorates Dextran Sodium Sulfate-Induced Ulcerative Colitis via Thymic Stromal Lymphopoietin in Mice

  AUTHORS: Keiichi Hiramoto, Kumi Orita, Yurika Yamate, Satoshi Yokoyama

  KEYWORDS: DSS-Induced Ulcerative Colitis, Atopic Dermatitis, Thymic Stromal Lymphopoietin, Dendritic Cell, T Helper 2 Cell, T Helper 17 Cell

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.5 No.3, March 23, 2017

  ABSTRACT: It has been reported that atopic dermatitis (AD) and ulcerative colitis are related. However, the mechanism underlying this association has not been clarified. We therefore explored how AD induces ulcerative colitis. We developed an AD mouse model (NC/Nga mice) with ulcerative colitis by administering dextran sodium sulfate (DSS) for five days. DSS-induced ulcerative colitis was deteriorated in our conventional AD mouse model compared with specific-pathogen-free (SPF) mice. The plasma levels of thymic stromal lymphopoietin (TSLP) and tumor necrosis factor-α increased the most in DSS-treated conventional mice. Furthermore, the expression of dendritic cells (DC), retinoid-related orphan receptor (ROR)γt (marker of T helper 17 cells [Th17]), interleukin (IL)-17, GATA binding protein 3 (GATA3) (marker of Th2), and IL-4 increased the most in the colon of the DSS-treated conventional mice compared with DSS-treated SPF mice. In addition, TSLP inhibitor (TSLP neutralizing antibody) did not exacerbate ulcerative colitis in DSS-treated conventional mice. These results indicate that TSLP/DC/Th2 and Th17 play major roles in the exacerbation of ulcerative colitis by AD.