RORγt protein modifications and IL-17-mediated inflammation

Ritesh Kumar, Arianne L. Theiss, K. Venuprasad

Research output: Contribution to journalReview articlepeer-review

Abstract

RORγt, the master transcription factor for cytokine interleukin (IL)-17, is expressed explicitly in Th17 cells, γδT cells, and type 3 innate lymphoid cells in mice and humans. Since dysregulated IL-17 expression is strongly linked to several human inflammatory diseases, the RORγt–IL-17 axis has been the focus of intense research. Recently, several studies have shown that RORγt is modified by multiple post-translational mechanisms, including ubiquitination, acetylation, SUMOylation, and phosphorylation. This review discusses how post-translational modifications modulate RORγt function and its turnover to regulate IL-17-driven inflammation. Broad knowledge of these pathways is crucial for a clear understanding of the pathogenic role of RORγt+IL-17+ cells and for the development of putative therapeutic strategies to target IL-17-driven diseases such as multiple sclerosis, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, and inflammatory bowel disease.

Original languageEnglish (US)
Pages (from-to)1037-1050
Number of pages14
JournalTrends in Immunology
Volume42
Issue number11
DOIs
StatePublished - Nov 2021

Keywords

  • IL-17
  • RORγt
  • Th17
  • autoimmune diseases
  • post-translational modifications

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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