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Positive and Negative Regulation of Th17 Cell Differentiation: Evaluating The Impact of RORC2

Mazdak Ganjalikhani Hakemi1, Kamran Ghaedi2, Vida Homayouni3

  • 1Cellular and Molecular Immunology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran ; Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Cell Journal
|March 11, 2014
PubMed
Abstract

Insights

Silencing RORC2 (Retinoid-related Orphan Receptor C2) effectively suppresses IL-17 and IL-23R in differentiating Th17 cells, highlighting RORC2 as a key target for inflammatory diseases.

Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • T helper 17 (Th17) cells are implicated in inflammatory and autoimmune conditions.
  • RORC2 (Retinoid-related Orphan Receptor C2) is a critical transcription factor for Th17 cell differentiation.
  • Targeting RORC2 offers a potential strategy to mitigate Th17-dependent inflammation.

Purpose of the Study:

  • To investigate the effect of RORC2 silencing on Th17 cell differentiation.
  • To analyze the time-dependent expression of RORC2, IL-17, and IL-23R during Th17 polarization.
  • To evaluate the efficacy of siRNA-mediated RORC2 knockdown.

Main Methods:

  • Naïve human CD4(+) T cells were isolated from cord blood.
  • Cells were polarized to Th17 using TGFß, IL-6, and IL-23 in serum-free medium.
  • RORC2 expression was silenced using a mixture of three specific siRNAs.
  • Gene and protein expression of RORC2, IL-17, and IL-23R were quantified via qRT-PCR, ELISA, and flow cytometry.

Main Results:

  • Significant time-dependent correlations were observed between RORC2 and IL-17/IL-23R expression (R=0.87-0.89, p<0.05).
  • RORC2 silencing led to a 99.3% suppression of IL-17 and a 77.2% decrease in IL-23R gene expression (p<0.05).

Conclusions:

  • RORC2 is a primary regulator of IL-17 and IL-23R gene expression during human Th17 cell differentiation.
  • Day 3 of differentiation represents a critical time point for Th17 development.
  • Silencing RORC2 presents a viable therapeutic approach for Th17-mediated inflammatory disorders.
Keywords:
IL-17IL-23RRORC2Th17siRNA

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