Mast cells in psoriatic skin are strongly positive for interferon‐gamma

L Ackermann, IT Harvima, J Pelkonen… - British Journal of …, 1999 - academic.oup.com
L Ackermann, IT Harvima, J Pelkonen, V Ritamäki‐Salo, A Naukkarinen, RJ Harvima…
British Journal of Dermatology, 1999academic.oup.com
The increased number and early activation of cutaneous mast cells is a typical feature of
psoriatic inflammation. Interferon‐gamma (IFN‐γ) is believed to be one of the important
mediators in the cytokine cascade of psoriasis. Human mast cells have been previously
reported to release various cytokines upon stimulation including interleukin (IL)‐4, IL‐5, IL‐
6, IL‐8, IL‐13 and tumour necrosis factor‐alpha. Here we report that human mast cells
synthesize also IFN‐γ at mRNA and protein level and that the number of IFN‐γ producing …
Abstract
The increased number and early activation of cutaneous mast cells is a typical feature of psoriatic inflammation. Interferon‐gamma (IFN‐γ) is believed to be one of the important mediators in the cytokine cascade of psoriasis. Human mast cells have been previously reported to release various cytokines upon stimulation including interleukin (IL) ‐4, IL‐5, IL‐6, IL‐8, IL‐13 and tumour necrosis factor‐alpha. Here we report that human mast cells synthesize also IFN‐γ at mRNA and protein level and that the number of IFN‐γ producing mast cells is significantly increased in the psoriatic skin. IFN‐γ immunoreactivity in mast cells was demonstrated by staining non‐lesional and lesional skin sections from 21 patients with psoriasis. Ten patients with atopic dermatitis (AD) and five healthy persons served as control groups. The percentage (mean ± SD) of IFN‐γ + mast cells in lesional compared with non‐lesional psoriatic skin was 67 ± 18% vs. 44 ± 17% (P< 0.0001, paired t‐test), respectively, but only 9 ± 6% vs. 10 ± 7% in corresponding skin samples of AD. In the skin of healthy controls, only 12 ± 12% of the mast cells were IFN‐γ +. Using immunoelectron microscopy, we confirmed the ultrastructural localization of IFN‐γ within the granules of mast cells in psoriatic skin. In addition, stimulation of a human mast cell line HMC‐1 with phorbol myristate acetate (PMA) (100 nmol/L) for periods of 2–24 h induced expression of IFN‐γ mRNA, which peaked at 24 h. When HMC‐1 cells were stimulated with PMA (100 nmol/L) for periods of 0–3 days, the cells released IFN‐γ protein, peaking on day 1. These results provide further evidence for the important role of mast cells in the pathogenesis of psoriasis.
Oxford University Press