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Updated: Apr 20, 2026

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
Published on: April 8, 2016
Experimentally induced psoriatic lesions associate with rapid but transient decrease in interleukin-33 immunostaining
Mireille-Maria Suttle1, Mattias Enoksson, Anna Zoltowska
1Department of Dermatology, University of Eastern Finland and Kuopio University Hospital, 70029 Kuopio, Finland.
Epidermal damage can trigger the Köbner reaction in psoriasis. This study found that interleukin-33 (IL-33) in the epidermis is linked to this reaction and may stimulate mast cells.
Area of Science:
- Dermatology
- Immunology
- Cell Biology
Background:
- The Köbner reaction is a phenomenon in psoriasis where skin lesions appear at sites of injury.
- Interleukin-33 (IL-33), an alarmin, is a potential mediator in inflammatory skin conditions like psoriasis.
Purpose of the Study:
- To investigate the role of epidermal interleukin-33 (IL-33) in the Köbner reaction of psoriasis.
- To determine if IL-33 released from damaged keratinocytes affects mast cells and other immune cells.
Main Methods:
- Tape stripping was used to induce minor epidermal damage in uninvolved psoriatic skin.
- Skin biopsies were collected at various time points (0 day, 2 h, 1 day, 3 days, 7 days) for immunohistochemistry.
- Keratinocyte cultures were used to assess IL-33 release upon cell damage, and its effect on mast cells and peripheral blood mononuclear cells was evaluated.
Main Results:
- Patients with a positive Köbner reaction showed reduced epidermal thickness and transiently decreased IL-33 immunostaining in biopsies compared to Köbner-negative patients.
- Damaged keratinocytes in culture released full-length IL-33.
- Low concentrations of recombinant human IL-33 (rh-IL-33) stimulated proliferation in LAD2 mast cells but not in psoriatic peripheral blood mononuclear cells.
Conclusions:
- Epidermal IL-33 levels are associated with the Köbner reaction in psoriasis.
- Released IL-33 may contribute to the inflammatory process by stimulating dermal mast cell proliferation.
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