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LL37/self-DNA complexes mediate monocyte reprogramming.

Aman Damara1, Joanna Wegner1, Emily R Trzeciak1

  • 1Department of Dermatology, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.

Clinical Immunology (Orlando, Fla.)
|June 23, 2024
PubMed
Summary
This summary is machine-generated.

Antimicrobial peptide LL37 and self-DNA trigger inflammation and epigenetic changes in monocytes, contributing to autoimmune diseases like psoriasis. Inhibiting KDM6A/B reversed these trained immunity effects, offering therapeutic potential.

Keywords:
LL37/self-DNA complexMetabolic and epigenetic modificationsMonocyte reprogrammingPsoriasis

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Area of Science:

  • Immunology
  • Epigenetics
  • Metabolic changes

Background:

  • LL37 and self-DNA complexes are implicated in autoimmune diseases such as psoriasis and lupus.
  • These complexes can induce lasting changes in myeloid cells, affecting immune responses.

Purpose of the Study:

  • To investigate the long-term metabolic and epigenetic effects of LL37/self-DNA complexes on monocytes.
  • To explore the role of KDM6A/B in the trained immune phenotype induced by LL37/self-DNA.

Main Methods:

  • Treatment of monocytes with LL37/self-DNA complexes.
  • Analysis of metabolic activity (glycolysis, oxidative phosphorylation) and cytokine release.
  • Assessment of KDM6A/B expression and functional inhibition.
  • Evaluation of effects on naïve CD4+ T cells.

Main Results:

  • LL37/self-DNA complexes induced heightened metabolic rates and pro-inflammatory cytokine release in monocytes, mimicking psoriatic monocytes.
  • KDM6A/B demethylase was upregulated in treated monocytes and those from psoriatic patients.
  • Inhibition of KDM6A/B reversed the trained immune phenotype, reducing inflammation and T cell induction.

Conclusions:

  • LL37/self-DNA-induced innate immune memory contributes to psoriasis pathogenesis.
  • KDM6A/B plays a critical role in mediating the trained immune response in monocytes.
  • Targeting KDM6A/B may offer a therapeutic strategy for psoriasis and related autoimmune conditions.