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SKI Expression Suppresses Pathogenic Th17 Cell Response and Mitigates Experimental Autoimmune Encephalomyelitis
Ping Li1,2,3, Zengli Guo1,2, Yisong Y Wan1,2
1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Frontiers in Immunology
|August 2, 2021
Summary
Targeting SKI protein can modulate pathogenic T helper 17 (Th17) cell function. This study reveals SKI
Area of Science:
- Immunology
- Cell Biology
- Neuroimmunology
Background:
- Pathogenic T helper 17 (Th17) cells drive autoimmune diseases.
- Transforming growth factor-β (TGFβ) signaling regulates Th17 differentiation via SKI.
- The role of SKI in TGFβ-independent pathogenic Th17 differentiation remains unclear.
Purpose of the Study:
- To investigate the role of SKI in pathogenic Th17 cell differentiation and function.
- To explore SKI as a therapeutic target for Th17-mediated autoimmune diseases.
Main Methods:
- Investigated SKI expression during pathogenic Th17 differentiation.
- Utilized ectopic SKI expression in T cells and a knock-in mouse model.
- Employed experimental autoimmune encephalomyelitis (EAE) and adoptive T cell transfer models.
Main Results:
- SKI expression is downregulated in pathogenic Th17 cells.
- Ectopic SKI expression inhibits pathogenic Th17 differentiation and prevents EAE.
- Induced SKI expression in differentiated Th17 cells reduces disease severity.
Conclusions:
- SKI plays a critical role in maintaining the pathogenic Th17 cell program.
- Targeting SKI offers a potential therapeutic strategy for autoimmune diseases like multiple sclerosis.
