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Updated: Dec 9, 2025

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Na&#239;ve CD4+ T Cells Using a TGF-&#946;-containing Protocol
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PPP2R2D suppresses IL-2 production and Treg function.

Wenliang Pan1, Amir Sharabi1, Andrew Ferretti1

  • 1Department of Medicine, Beth Israel Deaconess Medical Center (BIDMC) and Harvard Medical School, Boston, Masschusetts, USA.

JCI Insight
|September 8, 2020
PubMed
Summary
This summary is machine-generated.

The regulatory subunit PPP2R2D increases in T cells during systemic autoimmunity, decreasing IL-2 production. Removing PPP2R2D in T cells boosts IL-2 and reduces autoimmune symptoms.

Keywords:
Autoimmune diseasesAutoimmunityImmunologyPhosphoprotein phosphatasesT cells

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmunity

Background:

  • Protein phosphatase 2A (PP2A) is crucial in cellular processes and implicated in autoimmunity.
  • Decreased interleukin-2 (IL-2) production is a hallmark of systemic autoimmunity.
  • Specific regulatory subunits of PP2A may control IL-2 production and autoimmune responses.

Purpose of the Study:

  • To investigate the role of specific PP2A regulatory subunits in T cell function and autoimmunity.
  • To determine if PPP2R2D influences IL-2 production in systemic lupus erythematosus (SLE).
  • To explore the therapeutic potential of targeting PP2A regulatory subunits.

Main Methods:

  • Analysis of PPP2R2D levels in T cells from SLE patients.
  • Generation of mice with T cell-specific deletion of PPP2R2D.
  • Assessment of IL-2 production, gene expression, and CREB phosphorylation in T cells.
  • Evaluation of autoimmune phenotypes in mice upon TLR7 stimulation.
  • In vitro and in vivo functional assays for regulatory T cell (Treg) suppressive capacity.

Main Results:

  • PPP2R2D is upregulated in T cells from individuals with SLE and regulates IL-2 production.
  • T cell-specific deletion of PPP2R2D leads to increased IL-2 production due to open gene loci and high CREB phosphorylation.
  • Mice lacking T cell PPP2R2D exhibit reduced systemic autoimmunity following TLR7 stimulation.
  • Tregs maintain high suppressive function in vitro and in vivo, irrespective of PPP2R2D levels.

Conclusions:

  • PPP2R2D is a key regulator of IL-2 production and T cell-mediated autoimmunity.
  • Targeting specific PP2A regulatory subunits like PPP2R2D offers a potential strategy for developing function-specific immunotherapies.
  • This finding opens avenues for novel treatments for autoimmune diseases by modulating specific T cell functions.