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RORγt protein modifications and IL-17-mediated inflammation
Ritesh Kumar1, Arianne L Theiss2, K Venuprasad1
1Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX 75390, USA; Department of Immunology, UT Southwestern Medical Center, Dallas, TX 75390, USA; Harold C. Simmons Comprehensive Cancer Center, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Trends in Immunology
|October 12, 2021
Summary
RORγt, a key factor in IL-17 production, is regulated by post-translational modifications. Understanding these changes is vital for developing therapies for inflammatory diseases like psoriasis and multiple sclerosis.
Area of Science:
- Immunology
- Molecular Biology
Background:
- RORγt is the master transcription factor for interleukin-17 (IL-17), crucial in immune responses.
- Dysregulated IL-17 is implicated in various human inflammatory diseases.
Purpose of the Study:
- To review how post-translational modifications (PTMs) affect RORγt function.
- To explore the role of RORγt PTMs in regulating IL-17-driven inflammation.
Main Methods:
- Literature review of studies on RORγt post-translational modifications.
- Analysis of the impact of ubiquitination, acetylation, SUMOylation, and phosphorylation on RORγt.
Main Results:
- RORγt undergoes diverse PTMs, including ubiquitination, acetylation, SUMOylation, and phosphorylation.
- These PTMs modulate RORγt activity, protein stability, and IL-17 production.
Conclusions:
- Post-translational modifications are critical regulators of RORγt function and IL-17-mediated inflammation.
- Targeting RORγt PTMs offers potential therapeutic strategies for inflammatory conditions.
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