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Psoriasis Plays a Wild CARD

Elien Van Nuffel1, Inna S Afonina1, Rudi Beyaert1

  • 1Unit of Molecular Signal Transduction in Inflammation, Center for Inflammation Research, VIB, Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.

The Journal of Investigative Dermatology
|August 26, 2018
PubMed

Insights

Rare CARD14 gene mutations are linked to psoriasis. Researchers created mice with a specific mutation, demonstrating that CARD14 overactivation alone drives psoriasis development through the IL-17/IL-23 pathway.

Area of Science:

  • Immunology
  • Genetics
  • Dermatology

Background:

  • Autosomal mutations in CARD14 are associated with psoriasis susceptibility.
  • The precise pathogenic role of these CARD14 mutations remained unelucidated.

Purpose of the Study:

  • To investigate the pathogenic role of CARD14 gain-of-function mutations in psoriasis development.
  • To determine if CARD14 hyperactivation is sufficient to induce psoriasis-like pathology.

Main Methods:

  • Generation of genetically engineered mice carrying the patient-derived Card14ΔE138 gain-of-function mutation.
  • Analysis of immunopathogenic mechanisms and the role of the IL-17/IL-23 axis in the mutant mice.

Main Results:

  • Mice with the Card14ΔE138 mutation spontaneously developed psoriasis-like skin inflammation.
  • CARD14 hyperactivation alone was sufficient to trigger the observed immunopathogenic mechanisms.
  • The development of psoriasis in these mice was critically dependent on the IL-17/IL-23 signaling pathway.

Conclusions:

  • Gain-of-function mutations in CARD14 are pathogenic and sufficient to drive psoriasis.
  • The IL-17/IL-23 axis is a key mediator in CARD14-driven psoriasis.
  • This study provides a direct link between CARD14 mutations and psoriasis pathogenesis.

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