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Does molecular scarring in psoriasis exist? A review of the literature
Marta Kasprowicz-Furmańczyk1, Joanna Narbutt2, Adam Borzęcki3
1Department of Dermatology, Sexually Transmitted Diseases and Clinical Immunology, The University of Warmia and Mazury, Olsztyn, Poland.
Abstract:
Plaque psoriasis is a chronic inflammatory dermatosis characterized by a tendency to recur in the same locations after discontinuation of treatment. The implementation of therapy with drugs targeting cytokines like interleukin (IL) 17A (IL-17A) and IL-23 has revolutionized the treatment of psoriasis and enabled the achievement of skin without lesions. However, despite the clinical resolution of psoriatic eruptions, cells that maintain the local memory of the disease remain in the dermis and epidermis, constituting a kind of molecular scar. The cells responsible for maintaining memory in the skin of patients and influencing the rapid relapse of the disease after the triggering factor are primarily tissue resident memory T cells (TRM), but it seems that regulatory T lymphocytes (Treg), dendritic cells (DC), and Langerhans cells (LC) may also play an important role in this process. We reviewed the literature to explain the concept of molecular scarring in psoriasis, and to assess the effect of various therapies on immune memory.
Insights
Plaque psoriasis treatments can clear skin, but immune memory cells remain, causing rapid relapse. Understanding this "molecular scarring" is key to preventing psoriasis recurrence.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Plaque psoriasis is a chronic inflammatory skin disease known for recurring lesions.
- Biologic therapies targeting interleukin (IL)-17A and IL-23 have greatly improved treatment outcomes.
- Despite clinical clearance, disease-associated immune cells persist in the skin, forming a
- molecular scar
Purpose of the Study:
- To elucidate the concept of molecular scarring in psoriasis.
- To review the role of immune cells in maintaining psoriasis memory.
- To assess how therapies impact this immune memory.
Main Methods:
- Literature review.
- Analysis of immunological data related to psoriasis.
- Examination of therapeutic effects on cellular memory.
Main Results:
- Tissue-resident memory T cells (TRM) are primary drivers of psoriasis relapse.
- Regulatory T lymphocytes (Treg), dendritic cells (DC), and Langerhans cells (LC) may also contribute to memory.
- Therapies targeting IL-17A and IL-23 can achieve lesion-free skin but may not eliminate all memory cells.
Conclusions:
- Molecular scarring, driven by persistent immune cells like TRM, explains rapid psoriasis relapse.
- Understanding and targeting these memory cells is crucial for developing strategies to prevent disease recurrence.
- Further research is needed to fully characterize the role of various immune cells and the impact of therapies on long-term psoriasis memory.
