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Updated: Jan 19, 2026

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
Published on: October 25, 2024
REGγ controls Th17 cell differentiation and autoimmune inflammation by regulating dendritic cells
Lei Zhou1, Liangfang Yao1, Qing Zhang2
1Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, 500 Dongchuan Road, 200241, Shanghai, P. R. China.
REGγ deficiency in dendritic cells exacerbates autoimmune neuroinflammation by enhancing Interleukin-17A-producing helper T cell differentiation. This occurs through increased integrin αvβ8 expression, driven by impaired proteasomal degradation of IRF8.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Helper T (Th17) cells are crucial in autoimmune diseases.
- The innate immune system's role in triggering Th17 responses is not fully understood.
Purpose of the Study:
- To investigate the role of REGγ in autoimmune neuroinflammation.
- To elucidate the mechanism by which REGγ influences Th17 cell differentiation.
Main Methods:
- Experimental autoimmune encephalomyelitis (EAE) model in mice.
- Adoptive transfer of CD4+ T cells and dendritic cells (DCs).
- Analysis of protein degradation pathways and gene expression.
Main Results:
- REGγ-deficient mice showed worsened autoimmune neuroinflammation and increased Th17 polarization.
- Dendritic cells, not T cells, were responsible for the observed phenotype.
- REGγ deficiency led to increased integrin αvβ8 on DCs, promoting TGF-β1 maturation and Th17 development via IRF8 degradation.
Conclusions:
- REGγ-mediated proteasomal degradation of IRF8 in DCs is a key regulator of Th17 cell differentiation.
- This pathway influences the development of experimental autoimmune diseases.
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