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Mechanobiology of neutrophil inflammasome signaling in psoriasis

Yoshiaki Matsushima1, Samuel T Hwang2, Scott I Simon3

  • 1Department of Dermatology, University of California Davis School of Medicine, Sacramento, CA, USA; Department of Dermatology, Mie University, Tsu, Mie, Japan.

Current Opinion in Immunology
|October 18, 2025
PubMed

Insights

Polymorphonuclear neutrophils (PMN) amplify skin inflammation in psoriasis through mechanobiology. Targeting PMN mechanosignaling offers a novel therapeutic approach for psoriasis treatment.

Area of Science:

  • Immunology
  • Dermatology
  • Cell Biology

Background:

  • Psoriasis pathogenesis involves T cells and polymorphonuclear neutrophils (PMN).
  • The mechanobiology of PMN in skin inflammation is under-scrutinized.
  • PMN contribute to sustained skin inflammation and keratinocyte hyperproliferation.

Purpose of the Study:

  • To review the mechanobiology of PMN in amplifying skin inflammation in psoriasis.
  • To highlight PMN's role in the positive feedback loop of psoriatic disease.
  • To explore novel therapeutic strategies targeting PMN mechanosignaling.

Main Methods:

  • Review of literature on PMN function in psoriasis.
  • Analysis of PMN recruitment and activation mechanisms.
  • Discussion of mechanosignaling pathways in PMN.

Main Results:

  • PMN rolling and arrest in skin microcirculation are selectin- and β2-integrin-mediated.
  • PMN activation triggers NLRP3 inflammasome and NETosis, releasing inflammatory mediators.
  • These mediators drive keratinocyte proliferation and recruit more PMN, creating a feedback loop.

Conclusions:

  • PMN activation serves as a sensitive biomarker for psoriatic disease progression.
  • Targeting upstream PMN mechanosignaling pathways offers a novel therapeutic avenue.
  • This approach may overcome limitations of current cytokine-blocking therapies.

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