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SRC3 Is a Cofactor for RORγt in Th17 Differentiation but Not Thymocyte Development

Zhiheng He1, Jing Zhang1,2, Qian Du1

  • 1Department of Molecular Immunology, Beckman Research Institute of City of Hope, Duarte, CA 91010.

Journal of Immunology (Baltimore, Md. : 1950)
|December 21, 2018
PubMed

Insights

Steroid receptor coactivator 3 (SRC3) interacts with RORγt in Th17 cells, regulating their differentiation. SRC3 collaborates with SRC1 to control RORγt-dependent Th17 cell function.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Steroid receptor coactivators (SRCs) are crucial for gene transcription.
  • SRC family members, including SRC1 and SRC3, play roles in cellular regulation.
  • SRC1 was previously shown to interact with RORγt and regulate Th17 differentiation.

Purpose of the Study:

  • To investigate the role of SRC3 in Th17 cell function and its relationship with SRC1.
  • To determine if SRC3 interacts with RORγt in Th17 cells and its functional significance.

Main Methods:

  • Co-immunoprecipitation assays to assess protein interactions.
  • Analysis of Th17 cell differentiation in wild-type and mutant mice.
  • Induction of experimental autoimmune encephalomyelitis (EAE) to evaluate immune response.

Main Results:

  • Mouse SRC3 interacts with RORγt specifically in Th17 cells.
  • Mice lacking SRC3 (Src3 mice) showed impaired Th17 differentiation and EAE induction.
  • A RORγt mutation disrupting SRC3 interaction impaired Th17 differentiation but not thymocyte development.

Conclusions:

  • SRC3 is essential for RORγt-dependent Th17 cell differentiation.
  • SRC3 functions alongside SRC1 to regulate Th17 cell function.
  • SRC3 is not critical for RORγt-dependent thymocyte development.

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