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Related Concept Videos

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Antigens Involved in Adaptive Immunity01:26

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Related Experiment Video

Updated: Nov 2, 2025

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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USP19 Suppresses Th17-Driven Pathogenesis in Autoimmunity.

Jing Zhang1, Ronald J Bouch1, Maxim G Blekhman2

  • 1Department of Microbiology and Immunology, Wake Forest School of Medicine, Winston-Salem, NC; and.

Journal of Immunology (Baltimore, Md. : 1950)
|June 17, 2021
PubMed
Summary

The deubiquitinase USP19 suppresses pathogenic T helper 17 (Th17) cell differentiation and autoimmune disease. USP19 targets the transcription factor RORγt, offering new therapeutic strategies for autoimmune conditions.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmunity

Background:

  • T helper 17 (Th17) cells are key drivers of autoimmune diseases.
  • The plasticity of Th17 cells contributes to their pathogenic potential, but the underlying mechanisms are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms regulating Th17 cell plasticity and pathogenicity.
  • To identify novel therapeutic targets for autoimmune diseases by investigating the role of ubiquitination in Th17 pathogenesis.

Main Methods:

  • Investigated the role of the Th17 lineage transcription factor RORγt in regulating ubiquitination pathways.
  • Assessed the correlation between ubiquitination activity and Th17-mediated pathology in autoimmune models.
  • Examined the function of the deubiquitinase USP19 in Th17 differentiation and autoimmune pathogenesis in vitro and in vivo.
  • Determined the specific mechanism by which USP19 regulates RORγt activity.

Main Results:

  • RORγt directly upregulates genes in the ubiquitination pathway in pathogenic Th17 cells.
  • Increased ubiquitination activity correlates with Th17-related autoimmune pathology.
  • USP19 suppresses pathogenic Th17 differentiation and Th17-mediated pathogenesis.
  • USP19 deubiquitinates RORγt at lysine 313, disrupting its interaction with the coactivator SRC3.

Conclusions:

  • USP19 selectively inhibits the pathogenic potential of Th17 cells by modulating RORγt activity.
  • USP19 represents a promising therapeutic target for treating autoimmune diseases.