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Antisense oligonucleotides targeting IRF4 alleviate psoriasis.

Yanxia Yu1,2,3,3, Yirui Wang1,2,4, Weiwei Chen1,2,4

  • 1Department of Dermatology, the First Affiliated Hospital of Anhui Medical University, Hefei 230032, China.

Acta Pharmaceutica Sinica. B
|July 23, 2025
PubMed
Summary

Interferon regulatory factor 4 (IRF4) drives psoriasis inflammation by boosting IL-17A production in CD4+ T cells. Targeting IRF4 significantly reduced psoriatic symptoms in mouse models, suggesting it as a potential therapeutic target.

Keywords:
CD4EP300IL-17AIL-1βIL-23AIRF4PathogenesisPsoriasis

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Area of Science:

  • Immunology
  • Dermatology
  • Molecular Biology

Background:

  • Psoriasis pathogenesis involves immune imbalance and IL-17A overproduction by T cells.
  • The specific role of Interferon regulatory factor 4 (IRF4) in psoriasis remains uninvestigated.

Purpose of the Study:

  • To elucidate the role of IRF4 in the pathogenesis of psoriasis.
  • To explore IRF4 as a potential therapeutic target for psoriasis.

Main Methods:

  • Investigated IRF4 activity in psoriatic lesions from patients.
  • Utilized an Irf4 gene deletion mouse model and antisense oligonucleotides for pharmacological inhibition.
  • Assessed IL-17A production and CD4+ T cell populations.

Main Results:

  • IRF4 activity was elevated in psoriatic lesions, stimulated by IL-23A and IL-1β.
  • IRF4 binds to the EP300 promoter, increasing RORγt transcription and IL-17A secretion, forming an inflammatory cascade.
  • Targeting IRF4 ameliorated imiquimod-induced psoriatic-like symptoms and reduced IL-17A+ CD4+ T cells.

Conclusions:

  • IRF4 is a key driver of inflammation and exacerbation in psoriatic dermatitis.
  • Targeting IRF4 presents a promising therapeutic strategy for psoriasis.