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CTACK /CCL27 expression in psoriatic skin and its modification after administration of etanercept
Author(s) -
Campanati A.,
Goteri G.,
Simonetti O.,
Ganzetti G.,
Giuliodori K.,
Stramazzotti D.,
Morichetti D.,
Bernardini M.L.,
Mannello B.,
Fabris G.,
Offidani A.
Publication year - 2007
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2007.08200.x
Subject(s) - etanercept , medicine , psoriasis , dermatology , pharmacology , immunology , tumor necrosis factor alpha
Summary Background Tumour necrosis factor‐α upregulates the expression of a cutaneous T cell‐attracting chemokine (CTACK/CCL27), that promotes migration of cutaneous lymphocyte‐associated antigen‐positive lymphocytes into the skin. The role of CTACK/CCL27 in pathogenesis of psoriasis has recently been documented but no data are available at the present time on its modification in psoriatic cutaneous tissue after administration of etanercept. Objectives To evaluate modifications of CTACK/CCL27 expression in skin of patients with psoriasis after administration of etanercept and their relation with disease activity. Methods Twenty‐two patients with moderate to severe psoriasis underwent clinical, histological and immunohistochemical evaluations of disease activity at baseline and at 12 and 24 weeks after starting treatment with etanercept. Results All selected patients experienced an improvement of Psoriasis Area and Severity Index (PASI) score ( P < 0·001) and Dermatology Life Quality Index score ( P < 0·001) during the treatment. Skin histological abnormalities showed statistically significant modifications during treatment ( P < 0·001). Immunohistochemical expression of CTACK/CCL27 decreased significantly ( P < 0·001) and its relation with final PASI score was statistically significant ( P < 0·05); the pattern of distribution of CTACK/CCL27 immunoreactivity significantly moved from diffuse and predominantly suprabasal to basal ( P < 0·001) and the restoration of basal distribution of CTACK/CCL27 was also significantly related to clinical improvement of cutaneous disease ( P < 0·001). Conclusions Etanercept induces a clinical and histological improvement of psoriatic disease, promoting a reduction in CTACK/CCL27 cutaneous immunostaining and favouring the restoration of physiological CTACK/CCL27 epidermal expression. Moreover, CTACK/CCL27 reduction in cutaneous expression during administration of etanercept could be considered a favourable prognostic marker.