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Related Concept Videos

T Cell Types and Functions01:24

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Related Experiment Video

Updated: Apr 28, 2026

A Strategy for the Study of IL-9-Producing Lymphoid Cells in the Nippostrongylus brasiliensis Infection Model
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BCL6 controls Th9 cell development by repressing Il9 transcription.

Ribal Bassil1, William Orent1, Marta Olah1

  • 1Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115; and.

Journal of Immunology (Baltimore, Md. : 1950)
|June 1, 2014
PubMed
Summary

The transcriptional repressor BCL6 negatively regulates Th9 cell development and IL-9 production. BCL6

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Biology

Background:

  • BCL6 (B cell lymphoma 6) is a transcriptional repressor crucial for T follicular helper cell development.
  • BCL6 has been previously shown to inhibit Th2 cell differentiation.
  • The role of BCL6 in Th9 cell biology remains largely unexplored.

Purpose of the Study:

  • To investigate the regulatory role of BCL6 in the development and function of Th9 cells.
  • To elucidate the molecular mechanisms underlying BCL6-mediated regulation of IL-9 production.
  • To assess the impact of BCL6 on Th9 cell encephalitogenicity in experimental autoimmune encephalomyelitis.

Main Methods:

  • Analysis of BCL6 expression dynamics during Th9 cell polarization.
  • Gain- and loss-of-function studies using forced BCL6 expression and BCL6 knockdown in Th9 cells.
  • Chromatin immunoprecipitation (ChIP) assays to determine BCL6 and STAT5 binding to the Il9 promoter.
  • Histone mark analysis at the Il9 promoter.
  • IL-9 luciferase reporter assays.
  • In vivo studies using experimental autoimmune encephalomyelitis (EAE) models.

Main Results:

  • BCL6 expression is transiently downregulated during Th9 cell differentiation.
  • Forced BCL6 expression impairs Th9 cell differentiation and IL-9 production, while BCL6 knockdown enhances it.
  • BCL6 and STAT5 bind to adjacent sites in the Il9 promoter, with STAT5 associated with permissive histone marks and BCL6 with repressive marks.
  • BCL6 represses STAT5-mediated Il9 transactivation.
  • In EAE, forced BCL6 expression in Th9 cells reduces IL-9 and increases IFN-γ, exacerbating disease.

Conclusions:

  • BCL6 acts as a key negative regulator of Th9 cell development and IL-9 production.
  • The IL-2/JAK3/STAT5 signaling pathway controls BCL6 function in Th9 cells.
  • BCL6 influences Th9 cell encephalitogenicity, suggesting a role in autoimmune diseases like EAE.