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Updated: Aug 11, 2026

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
Published on: April 8, 2016
Epidermal interleukin 1 alpha functional activity and interleukin 8 immunoreactivity are increased in patients with
E R Hansen1, G L Vejlsgaard, S Lisby
1Department of Dermatology, Rigshospitalet, Copenhagen, Denmark.
Insights
This study found increased levels of interleukin-1 alpha in cutaneous T-cell lymphoma (CTCL) epidermis, suggesting its role in CTCL pathogenesis. This elevated interleukin-1 alpha is biologically active and induced by T-cell lymphokines.
Area of Science:
- Dermatology
- Immunology
- Oncology
Background:
- Epidermal interleukin-1 (IL-1) involvement in cutaneous T-cell lymphoma (CTCL) pathogenesis is suggested but conflicting.
- Previous studies lack combined immunohistochemistry and functional activity assessments.
Purpose of the Study:
- To investigate epidermal interleukin-1 levels in CTCL patients.
- To combine immunohistochemistry and functional assays to clarify IL-1's role in CTCL.
- To explore the relationship between IL-1 alpha and IL-8 in CTCL epidermis.
Main Methods:
- Immunohistochemistry, enzyme-linked immunosorbent assays (ELISAs), and thymocyte co-stimulation assays were used.
- Epidermal cell cultures from CTCL patients and healthy individuals were analyzed.
- Functional activity of IL-1 alpha was assessed using thymocyte assays.
Main Results:
- A significant, albeit small, increase in interleukin-1 alpha (IL-1 alpha) protein release was observed in CTCL epidermis compared to normal epidermis.
- Keratinocytes were identified as the primary source of IL-1 alpha in the epidermis.
- Elevated interleukin-8 (IL-8) immunoreactivity was found in CTCL epidermis, correlating with increased IL-1 alpha.
Conclusions:
- Elevated epidermal IL-1 alpha and IL-8 levels in CTCL suggest their involvement in the disease.
- T-cell-derived lymphokines likely induce the enhanced release of IL-1 alpha in CTCL epidermis.
- This research clarifies the role of IL-1 alpha in CTCL pathogenesis.
Abstract:
Previous studies have suggested that epidermal-derived interleukin-1 is involved in the pathogenesis of cutaneous T-cell lymphoma (CTCL); however, the findings are conflicting and studies that combine immunohistochemistry and functional activity have not been performed. We investigated the interleukin-1 level in epidermis of patients with cutaneous T-cell lymphoma using both immunohistochemistry, enzyme-linked immunosorbent assays, and the thymocyte co-stimulation assay. Using supernatants obtained from epidermal cell cultures, we found a significant but small increase of interleukin 1 alpha protein release from involved CTCL epidermis compared to normal epidermis from healthy individuals. Both keratinocytes and leukocytes could release interleukin-1 alpha, but the majority was derived from the keratinocytes. Interleukin-1 beta protein was not detectable. In the thymocyte assay, interleukin-1 alpha was found to be biologically active. When lymphokines derived from a T-cell clone obtained from involved CTCL skin were co-cultured with epidermal cells, an enhanced release of epidermal interleukin-1 alpha could be demonstrated. Because interleukin 1 alpha was increased, we investigated the presence of interleukin 1-inducible keratinocyte-derived interleukin 8 and found it increased in CTCL epidermis compared to normal epidermis from healthy individuals. This study demonstrated an elevated epidermal IL-1 alpha level and IL-8 immunoreactivity in CTCL epidermis, which suggests that this elevated level is induced by lymphokines released from activated T cells.
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