CD30 ligand is a target for a novel biological therapy against colitis associated with Th17 responses

Xun Sun, Hisakata Yamada, Kensuke Shibata, Hiromi Muta, Kenzaburo Tani, Eckhard R. Podack, Yoichiro Iwakura, Yasunobu Yoshikai

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32 Citations (Scopus)

Abstract

We have previously found that CD30 ligand (CD30L; CD153)/CD30 signaling executed by the T-T cell interaction plays a critical role in Th17 cell differentiation, at least partly via downregulation of IL-2 production. In this study, we investigated the role of CD30L in the development of colitis experimentally induced by dextran sulfate sodium (DSS), in which IL-17A is involved in the pathogenesis. CD30L-/- mice were resistant to both acute colitis induced by administration of 3 to ∼5% DSS and to chronic colitis induced by administration of 1.5% DSS on days 0-5, 10-15, and 20-25 as assessed by weight loss, survival rate, and histopathology. The levels of IFN-γ, IL-17A, and IL-10 were significantly lower but the IL-2 level higher in the lamina propria T lymphocytes of CD30L-/- mice than those in lamina propria T lymphocytes of wild-type mice after DSS administration. Soluble murine CD30-Ig fusion protein, which was capable of inhibiting Th17 cell differentiation in vitro, ameliorated both types of DSS-induced colitis in wild-type mice. Modulation of CD30L/CD30 signaling by soluble CD30 could be a novel biological therapy for inflammatory diseases associated with Th17 responses.

Original languageEnglish
Pages (from-to)7671-7680
Number of pages10
JournalJournal of Immunology
Volume185
Issue number12
DOIs
Publication statusPublished - Dec 15 2010

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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    Sun, X., Yamada, H., Shibata, K., Muta, H., Tani, K., Podack, E. R., Iwakura, Y., & Yoshikai, Y. (2010). CD30 ligand is a target for a novel biological therapy against colitis associated with Th17 responses. Journal of Immunology, 185(12), 7671-7680. https://doi.org/10.4049/jimmunol.1002229