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

Xun Sun1, Hisakata Yamada, Kensuke Shibata

  • 1Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.

Journal of Immunology (Baltimore, Md. : 1950)
|November 12, 2010
PubMed

Insights

CD30 ligand (CD30L) deficiency protects against dextran sulfate sodium (DSS)-induced colitis in mice. This resistance is linked to altered cytokine profiles and suggests CD30L/CD30 signaling as a therapeutic target for inflammatory diseases.

Area of Science:

  • Immunology
  • Gastroenterology
  • Cellular Biology

Background:

  • CD30 ligand (CD30L)/CD30 signaling is crucial for T helper 17 (Th17) cell differentiation.
  • Th17 cells and IL-17A play a role in the pathogenesis of dextran sulfate sodium (DSS)-induced colitis.

Purpose of the Study:

  • To investigate the role of CD30L in the development of DSS-induced colitis.
  • To explore the therapeutic potential of modulating CD30L/CD30 signaling in inflammatory diseases.

Main Methods:

  • Utilized CD30L knockout (CD30L(-/-)) and wild-type mice in acute and chronic DSS-induced colitis models.
  • Assessed colitis severity through weight loss, survival rates, and histopathology.
  • Analyzed cytokine levels (IFN-γ, IL-17A, IL-10, IL-2) in lamina propria T lymphocytes.
  • Administered soluble murine CD30-Ig fusion protein to wild-type mice.

Main Results:

  • CD30L(-/-) mice exhibited resistance to both acute and chronic DSS-induced colitis.
  • Compared to wild-type mice, CD30L(-/-) mice showed lower levels of IFN-γ, IL-17A, and IL-10, but higher IL-2 levels in lamina propria T lymphocytes after DSS administration.
  • Soluble CD30-Ig fusion protein ameliorated DSS-induced colitis in wild-type mice, consistent with its in vitro Th17 cell differentiation inhibitory effect.

Conclusions:

  • CD30L plays a significant role in the pathogenesis of DSS-induced colitis.
  • Modulating CD30L/CD30 signaling via soluble CD30 represents a potential novel biological therapy for Th17-associated inflammatory diseases.

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