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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
Summary
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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