JSI-124 inhibits IgE production in an IgE B cell line

Biochem Biophys Res Commun. 2017 Jan 29;483(1):669-673. doi: 10.1016/j.bbrc.2016.12.085. Epub 2016 Dec 14.

Abstract

IgE is a key effector molecule in atopic diseases; however, the regulation mechanisms of IgE production in IgE B cells remain poorly understood. In the present study, we demonstrate that JSI-124 (cucurbitacin I), a selective STAT3 inhibitor, selectively inhibits production of IgE by a human IgE B cell line, CRL-8033 cells, while does not affect the IgG production by IgG B cell lines. In the aspect of molecular mechanism, we found that Igλ, but not Ighe, gene expression was suppressed by JSI-124. The above effects of JSI-124 were not mediated by affecting cellular proliferation or apoptosis. Furthermore, multiple B cell differentiation-related genes expression was not significantly affected by JSI-124. Taken together, we demonstrate a potential strategy of therapeutically suppressing IgE production without affecting IgG production in atopic patients.

Keywords: Atopic diseases; IgE; JSI-124.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • B-Lymphocytes / drug effects*
  • B-Lymphocytes / immunology
  • Cell Differentiation / drug effects
  • Cell Line
  • Cell Proliferation
  • Gene Expression / drug effects
  • Genes, Immunoglobulin / drug effects
  • Humans
  • Immunoglobulin E / biosynthesis*
  • Immunoglobulin E / genetics
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin G / genetics
  • STAT3 Transcription Factor / antagonists & inhibitors
  • Triterpenes / pharmacology*

Substances

  • Immunoglobulin G
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Triterpenes
  • Immunoglobulin E
  • cucurbitacin I