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Updated: Jan 20, 2026

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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Splicing factor SRSF1 controls T cell hyperactivity and systemic autoimmunity.

Takayuki Katsuyama1, Hao Li1, Denis Comte1,2

  • 1Division of Rheumatology and Clinical Immunology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

The Journal of Clinical Investigation
|September 6, 2019
PubMed
Summary

Serine/arginine-rich splicing factor 1 (SRSF1) deficiency in T cells drives systemic autoimmunity and lupus by promoting T cell activation. Restoring SRSF1 may offer a therapeutic strategy for lupus patients.

Keywords:
AutoimmunityCytokinesImmunologyLupusT cells

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by hyperactive T cells.
  • Serine/arginine-rich splicing factor 1 (SRSF1) is an RNA-binding protein crucial for gene expression.
  • Reduced SRSF1 levels in T cells correlate with SLE severity, but its role is unclear.

Purpose of the Study:

  • To investigate the function of SRSF1 in T cell physiology and its involvement in SLE pathogenesis.
  • To elucidate the molecular mechanisms by which SRSF1 regulates T cell activation.
  • To evaluate SRSF1 as a potential therapeutic target for lupus.

Main Methods:

  • Generated T cell-specific Srsf1-deficient mice to study autoimmunity.
  • Analyzed T cell activation, cytokine production, and gene expression profiles.
  • Investigated the mechanistic target of rapamycin (mTOR) pathway and PTEN expression.
  • Assessed the therapeutic potential of rapamycin and SRSF1 overexpression in SLE models.

Main Results:

  • Srsf1-deficient mice developed systemic autoimmunity and lupus nephritis with increased activated T cells and pro-inflammatory cytokines.
  • Mechanistically, SRSF1 deficiency led to enhanced mTOR pathway activity and reduced PTEN expression.
  • Rapamycin treatment suppressed T cell inflammation and alleviated autoimmunity in deficient mice.
  • SRSF1 overexpression restored PTEN levels, inhibited mTORC1, and reduced cytokine production in SLE T cells.

Conclusions:

  • SRSF1 plays a critical role in restraining T cell activation and preventing autoimmune disease development.
  • SRSF1 deficiency contributes to lupus pathogenesis through mTOR pathway dysregulation.
  • SRSF1 represents a novel therapeutic target for treating systemic lupus erythematosus.