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The tumour necrosis factor-alpha inhibitor adalimumab rapidly reverses the decrease in epidermal Langerhans cell

K B Gordon¹, B K Bonish, T Patel

¹Department of Internal Medicine, Division of Dermatology, Loyola University Medical Center, Maywood, IL 60153, USA.

The British Journal of Dermatology

|October 18, 2005

Summary

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Psoriatic plaques show a rapid loss of epidermal Langerhans cells (LCs), which is reversed by adalimumab treatment. This study reveals a new understanding of psoriasis immunopathology and anti-tumour necrosis factor (TNF)-alpha therapy mechanisms.

Area of Science:

Dermatology
Immunology
Pathophysiology

Background:

The exact pathophysiology of psoriasis remains unclear.
The mechanism of action for biological agents targeting tumour necrosis factor (TNF)-alpha in psoriasis treatment is unknown.

Purpose of the Study:

To investigate cellular changes in psoriatic plaques after adalimumab administration.
To elucidate the mechanism of action of adalimumab in treating psoriasis.

Main Methods:

Sequential biopsies from 13 psoriasis patients treated with adalimumab were analyzed for epidermal Langerhans cell (LC) density.
A SCID-Hu animal model was used to study LC density changes in acute psoriatic lesions.

Main Results:

Untreated psoriatic plaques had significantly lower epidermal LC density compared to normal skin.

Related Experiment Videos

Adalimumab treatment rapidly increased epidermal LC density in psoriatic plaques, starting by day 7.

Acute psoriatic lesion formation in the SCID-Hu model was associated with a loss of epidermal LCs.

Conclusions:

Psoriatic lesions are characterized by a rapid loss of epidermal LCs, which persists in chronic plaques.
Adalimumab treatment leads to a rapid restoration of epidermal LC density, offering new insights into its mechanism of action.