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Endothelin regulates function of IL-17-producing T cell subset.

Kensuke Tanaka1, Kento Yoshioka2, Koichiro Tatsumi3

  • 1Department of Biochemistry and Molecular Pharmacology, Graduate School of Medicine, Chiba University, Chiba 2608670, Japan; Department of Respirology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.

Life Sciences
|February 18, 2014
PubMed
Summary

Endothelin (ET) receptor blocker BQ123 significantly inhibits interleukin-17 (IL-17) production by Th17 cells, suggesting potential for multiple sclerosis treatment.

Keywords:
ET-1IL-17Multiple sclerosisTh17

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Area of Science:

  • Immunology
  • Neuroscience
  • Pharmacology

Background:

  • Endothelin (ET) has diverse roles in pathology, but its link to autoimmune diseases is unclear.
  • Interleukin-17 (IL-17) is implicated in the pathogenesis of multiple sclerosis (MS).

Purpose of the Study:

  • To investigate the effect of ET receptor blockers on IL-17 production by T lymphocytes.
  • To explore the role of ET/ETA signaling in IL-17 production by Th17 cells.

Main Methods:

  • Lymph node cells from MOG35-55-immunized mice were stimulated in vitro with MOG35-55 and ET receptor blockers (BQ123 for ETA, BQ788 for ETB).
  • Naïve T cells underwent in vitro Th17 differentiation to assess ET-mediated IL-17 production during differentiation and activation.

Main Results:

  • BQ123 significantly inhibited MOG35-55-induced IL-17 production, while BQ788 had no effect.
  • BQ123 reduced the frequency of IL-17-producing CD4(+) T cells but did not affect Th17 differentiation.
  • Post-differentiation, BQ123 significantly inhibited IL-17 production upon T cell activation.

Conclusions:

  • ET/ETA signaling is critical for IL-17 production in Th17 cells.
  • BQ123 shows promise as a potential therapeutic agent for multiple sclerosis.