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Published on: April 20, 2016
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.
Abstract:
Psoriasis is an inflammatory disease that arises in genetically predisposed individuals. Chronic skin lesions that contain activated immune cells can persist for years. Systemic inhibition of TNF, IL-17 and IL-23 cytokines has revolutionized psoriasis care during the recent decades. Unfortunately, local relapse of disease is common at previously inflamed sites after cessation of treatment. This highlights that fundamental pathologic alterations of the affected tissues are not completely resolved during clinical remission. Here, we present arguments for a local disease memory located in both dermis and epidermis in psoriasis skin. We decipher different cellular components and intercellular crosstalk that sustain local disease memory and amplify disease relapse in human psoriasis. Decrypting the mechanisms underlying the establishment and persistence of pathogenic memory cells in resolved psoriasis may provide new therapeutic perspectives aimed at long-term remission of psoriasis.
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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