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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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Related Experiment Video

Updated: Jun 3, 2025

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
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Insulin Sensitivity Controls Activity of Pathogenic CD4+ T Cells in Rheumatoid Arthritis.

Malin C Erlandsson1,2, Eric Malmhäll-Bah1, Venkataragavan Chandrasekaran1

  • 1Department of Rheumatology and Inflammation Research, Institute of Medicine, University of Gothenburg, 41346 Gothenburg, Sweden.

Cells
|January 8, 2025
PubMed
Summary
This summary is machine-generated.

Insulin exposure induces T cell senescence and suppresses immune function in rheumatoid arthritis (RA) patients with hyperinsulinemia. Janus kinase inhibitors (JAKi) may enhance these insulin effects, promoting the clearance of pathogenic T cells in RA.

Keywords:
CD4+ cellsarthritisinsulininterferonsenescence

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Area of Science:

  • Immunology
  • Endocrinology
  • Rheumatology

Background:

  • Hyperinsulinemia links obesity, dyslipidemia, and type 2 diabetes (T2D).
  • The impact of insulin on T cell function in rheumatoid arthritis (RA) autoimmunity is not fully understood.

Purpose of the Study:

  • To investigate the effects of insulin exposure on T cell function in the context of RA.
  • To explore the role of insulin in T cell senescence and immune suppression.

Main Methods:

  • Analysis of CD4+ T cell glycolytic index and insulin receptor substrate transcription.
  • Flow cytometry to assess cell cycle arrest, DNA content, and DNA damage (γH2AX).
  • Measurement of Interferon-gamma (IFNγ) production and senescence-associated secretome.

Main Results:

  • Insulin levels correlated with CD4+ T cell glycolytic index in RA patients, but suppressed insulin receptor substrates.
  • Insulin exposure induced T cell senescence, DNA damage, and suppressed IFNγ production.
  • Janus kinase inhibitors (JAKi) enhanced insulin signaling, T cell senescence, and promoted T cell clearance in RA patients.

Conclusions:

  • Insulin exerts immunosuppressive effects by inducing T cell senescence and inhibiting IFNγ production.
  • JAKi may potentiate insulin's effects, aiding in the elimination of pathogenic CD4+ T cells in RA.