Regulation of treg functions by the ubiquitin pathway

Elena Montauti, Deyu Fang*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

Abstract

Regulatory T (Tregs) cells, required to maintain immune homeostasis, have significant power in disease outcomes. Treg dysfunction, predominantly characterized by the loss of the master transcription factor FoxP3 and the acquisition of Teff-like phenotypes, can promote autoimmunity as well as enhance anti-tumor immunity. As FoxP3 expression and stability are pinnacle for Treg suppressive functions, understanding the pathways that regulate FoxP3 is crucial to ascertain Treg-mediated therapies for autoimmune diseases and cancer. Mechanisms controlling FoxP3 expression and stability range from transcriptional to posttranslational, revealing multiple therapeutic opportunities. While many of the transcriptional pathways have been explored in detail, a recent surge in interest on the posttranslational mechanisms regulating FoxP3 has arisen. Particularly, the role of ubiquitination on Tregs both directly and indirectly involving FoxP3 has gained interest. Here, we summarize the current knowledge on ubiquitin-dependent, FoxP3-mediated control of Treg function as it pertains to human diseases.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer
Pages47-62
Number of pages16
DOIs
StatePublished - 2021

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1278
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Keywords

  • Deubiquitination
  • E3 ligase
  • FoxP3
  • Treg
  • Ubiquitin

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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