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Updated: Jan 22, 2026

The MUB40 Peptide for Use in Detecting Neutrophil-Mediated Inflammation Events
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CYLD Limits Neutrophil-Driven Psoriatic Inflammation.

Zhenzong Fa1, Zeping Huang2, Yi Shang3

  • 1Department of Dermatology, the Sixth Medical Center, Chinese PLA General Hospital, Beijing, 100048, China.

Inflammation
|January 20, 2026
PubMed
Summary

The deubiquitinase CYLD suppresses psoriasis by inhibiting neutrophil activation and NETs formation. Activating CYLD could be a new psoriasis treatment.

Keywords:
CYLDNeutrophilNeutrophil extracellular traps.Psoriasis

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Area of Science:

  • Dermatology
  • Immunology
  • Molecular Biology

Background:

  • The deubiquitinase CYLD's role in psoriasis pathogenesis is unclear.
  • CYLD is implicated in tumors and inflammatory diseases.

Purpose of the Study:

  • Investigate CYLD's function and regulation in psoriasis.
  • Determine CYLD's impact on psoriasiform inflammation.

Main Methods:

  • Analyzed CYLD expression in patient samples and an imiquimod-induced mouse model.
  • Utilized Cyld knockout mice for histopathology, immunohistochemistry, RNA sequencing, and immunofluorescence.
  • Employed bioinformatics (CIBERSORT, WGCNA) to explore CYLD-neutrophil pathway associations.

Main Results:

  • CYLD was upregulated in psoriatic skin lesions.
  • Cyld deficiency exacerbated psoriasiform symptoms, including epidermal thickening and neutrophil infiltration.
  • CYLD deficiency increased neutrophil extracellular traps (NETs) formation and NF-κB pathway activation.
  • Bioinformatics linked CYLD to neutrophil migration and activation pathways.

Conclusions:

  • CYLD negatively regulates psoriasis by inhibiting NF-κB-mediated neutrophil activation and NETs formation.
  • Targeted CYLD activation presents a potential therapeutic strategy for psoriasis.