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Engaging the PD-1 pathway in systemic sclerosis attenuates inflammation-driven fibrosis.

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Modulating the programmed cell death protein 1 (PD-1) pathway reduces inflammation and fibrosis in diffuse cutaneous systemic sclerosis (dcSSc) models. This suggests targeting the PD-1 axis offers a new therapeutic strategy for dcSSc.

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Area of Science:

  • Immunology
  • Dermatology
  • Fibrosis Research

Background:

  • Diffuse cutaneous systemic sclerosis (dcSSc) is characterized by immune activation and fibrosis.
  • The programmed cell death protein 1 (PD-1) pathway plays a role in immune regulation.
  • Understanding PD-1's impact on dcSSc pathogenesis is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the role of the PD-1 pathway in immune activation and fibrosis in dcSSc.
  • To evaluate the therapeutic potential of modulating the PD-1 pathway in dcSSc.

Main Methods:

  • Analysis of serum and skin biopsies from dcSSc patients and healthy controls (HCs).
  • In vitro stimulation of peripheral blood mononuclear cells (PBMCs) and fibroblasts with PD-1:Fc and anti-PD-1 antibodies.
  • Characterization of PD-1-positive (PD-1pos) and PD-1-negative (PD-1neg) T cells.
  • In vivo studies using a murine bleomycin-induced pulmonary fibrosis model.

Main Results:

  • Elevated soluble and cellular PD-1 levels were observed in dcSSc patients compared to HCs.
  • PD-1:Fc treatment downregulated extracellular matrix (ECM) protein secretion and inflammatory cytokine production in TGF-β-stimulated fibroblasts.
  • PD-1pos SSc T cells exhibited a more regulatory transcriptional profile.
  • In vivo administration of PD-1:Fc inhibited lung fibrosis development and profibrotic cytokine production.

Conclusions:

  • Modulation of the PD-1/PD-Ligand 1 axis attenuated inflammation and ECM production in dcSSc models.
  • PD-1:Fc treatment reduced systemic inflammation and pulmonary fibrosis in a mouse model.
  • Targeting the PD-1 axis represents a promising novel therapeutic strategy for dcSSc.