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PP2A dysfunction mediated by PPP2R1A deficiency drives cGAS-STING-dependent hyperinflammation in SLE CD14+ monocytes.

Xuan Fang1,2, Xi Wen1, Hong Zhang2

  • 1Department of Rheumatology and Immunology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, Anhui, China.

Clinical Rheumatology
|January 25, 2026
PubMed
Summary

Protein phosphatase 2A (PP2A) dysfunction drives systemic lupus erythematosus (SLE) hyperinflammation by impairing monocyte immune responses. Restoring PP2A activity with FTY720 offers a potential therapeutic strategy for SLE immunomodulation.

Keywords:
Cyclic GMP-AMP synthaseInnate immunityProtein phosphatase 2AStimulator of interferon response cGAMP interactor 1Systemic lupus erythematosus

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Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Systemic lupus erythematosus (SLE) is characterized by a hyperinflammatory response in monocytes.
  • The precise mechanisms underlying this aberrant innate immune activation remain incompletely understood.
  • Protein phosphatase 2A (PP2A) is a key regulator of cellular processes, but its role in SLE pathogenesis is unclear.

Purpose of the Study:

  • To investigate the role of Protein Phosphatase 2A (PP2A) dysfunction in the hyperinflammatory response of systemic lupus erythematosus (SLE) monocytes.
  • To elucidate the functional link between PP2A subunit dysregulation, reduced enzymatic activity, and aberrant innate immune activation via the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon response cGAMP interactor 1 (STING) pathway.
  • To evaluate the therapeutic potential of modulating PP2A activity in SLE monocytes.

Main Methods:

  • Isolated CD14+ monocytes from 88 SLE patients and 40 healthy controls (HCs).
  • Analyzed PP2A subunit mRNA expression, PP2A phosphatase activity, and inhibitory phosphorylation (PP2Ac-Y307).
  • Modulated PP2A activity pharmacologically (LB-100 inhibition in HCs, FTY720 activation in SLE) and assessed cGAS-STING pathway activation, interferon-stimulated gene (ISG) expression, and cytokine secretion.

Main Results:

  • SLE monocytes showed decreased PPP2R1A expression, reduced PP2A activity, and increased PP2Ac-Y307 phosphorylation.
  • PP2A inhibition in HCs monocytes amplified cGAS-STING-dependent ISG expression and cytokine release, mimicking SLE phenotype.
  • FTY720-mediated PP2A activation in SLE monocytes significantly reduced the exaggerated immune response.

Conclusions:

  • PP2A hypofunction is a critical pathogenic driver in SLE monocytes, contributing to hyperinflammation.
  • The downregulation of PPP2R1A and subsequent reduction in PP2A activity are key pathological mechanisms.
  • Restoring PP2A activity, for example, with the agonist FTY720, effectively mitigates dysregulated innate immune responses, presenting a promising therapeutic strategy for SLE.