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Updated: Aug 9, 2026
Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
Published on: April 8, 2016
Impaired Langerhans cell migration in psoriasis
Marie Cumberbatch1, Minal Singh, Rebecca J Dearman
1Syngenta Central Toxicology Laboratory, Macclesfield, Cheshire, SK10 4TJ, England, UK.
Insights
Psoriasis patients show impaired epidermal Langerhans cell (LC) migration. This defect in LC function, despite normal cell appearance, suggests a key role in psoriasis pathogenesis.
Area of Science:
- Immunodermatology
- Cutaneous Immunology
Background:
- Psoriasis is a chronic inflammatory skin disease.
- Langerhans cells (LCs) are critical immune cells in the epidermis, involved in initiating immune responses.
- Systemic effects on LC function in psoriasis are not fully understood.
Purpose of the Study:
- To investigate systemic effects of psoriasis on epidermal LC function.
- To specifically assess the migratory capacity of LCs from uninvolved psoriatic skin.
Main Methods:
- Comparison of LC frequency and morphology in uninvolved psoriatic skin versus normal skin.
- Assessment of LC mobilization in response to chemical allergens, TNF-alpha, and IL-1beta.
- Evaluation of receptor expression for IL-1beta and TNF-alpha on LCs.
- Analysis of induced cutaneous cytokine expression.
Main Results:
- Epidermal LCs in uninvolved psoriatic skin had normal frequency and morphology.
- LC mobilization was significantly impaired in response to stimuli like TNF-alpha and IL-1beta.
- This impaired migration was observed despite comparable inflammatory reactions in patients and controls.
- Altered expression of cytokine receptors or induced cytokine expression did not explain the migration defect.
Conclusions:
- Psoriasis is associated with a consistent defect in epidermal LC function, specifically their migration.
- This impaired LC migration may be a crucial factor in the pathogenesis of psoriasis.
- Further research is needed to fully elucidate the dynamics of LC migration and turnover in psoriasis.
Abstract:
We have examined whether psoriasis is associated with systemic effects on epidermal Langerhans cell (LC) function and, specifically, the migration of LCs from the skin. Compared with normal skin, the frequency and morphology of epidermal LCs in uninvolved skin from patients with psoriasis was normal. However, mobilization of these cells in response to stimuli that normally induce migration (chemical allergen, tumor necrosis factor alpha [TNF-alpha], and interleukin-1beta [IL-1beta]) was largely absent, despite the fact that treatment with TNF-alpha and IL-1beta was associated with comparable inflammatory reactions in patients and controls. The failure of LC migration from uninvolved skin was not attributable to altered expression of receptors for IL-1beta or TNF-alpha that are required for mobilization, nor was there an association with induced cutaneous cytokine expression. Although a role for altered dynamics of LC migration/turnover has not been formally excluded, these data reveal a very consistent decrement of LC function in psoriasis that may play a decisive role in disease pathogenesis.
