Cellular scars and local crosstalk in relapsing psoriasis: an example of a skin sticking disease

Irène Gallais Sérézal1,2, Stanley Cheuk3,4, Elisa Martini1

  • 1Department of Medicine, Unit of Rheumatology Karolinska Institutet Solna, Stockholm, Sweden.

Insights

Psoriasis relapse may stem from a localized "disease memory" in skin tissues. Understanding this memory in immune cells could lead to long-term psoriasis remission.

Area of Science:

  • Immunodermatology
  • Pathogenesis of Psoriasis
  • Tissue Memory

Background:

  • Psoriasis is a chronic inflammatory skin disease.
  • Current systemic therapies targeting TNF, IL-17, and IL-23 are effective but often lead to local relapse.
  • Persistent pathological alterations in skin suggest unresolved disease processes.

Purpose of the Study:

  • To investigate the existence of local disease memory in psoriasis skin.
  • To identify cellular and molecular mechanisms sustaining this memory.
  • To explore therapeutic strategies for long-term psoriasis remission.

Main Methods:

  • Analysis of cellular components in dermis and epidermis of psoriasis skin.
  • Investigation of intercellular crosstalk sustaining disease memory.
  • Deciphering mechanisms of pathogenic memory cell establishment and persistence.

Main Results:

  • Evidence presented for local disease memory in both dermal and epidermal compartments of psoriasis skin.
  • Identification of specific cellular players and their interactions involved in memory formation.
  • Understanding how these mechanisms contribute to disease relapse.

Conclusions:

  • Psoriasis pathogenesis involves a localized disease memory within the skin.
  • This memory, sustained by cellular crosstalk, drives disease relapse.
  • Targeting these memory mechanisms offers potential for durable psoriasis remission.

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