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Etanercept restores a differentiated keratinocyte phenotype in psoriatic human skin: a morphological study
Author(s) -
Donetti Elena,
Gualerzi Alice,
Ricceri Federica,
Pescitelli Leonardo,
Bedoni Marzia,
Prignano Francesca
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2012.01518.x
Subject(s) - involucrin , keratinocyte , occludin , keratin , desmoglein , desmosome , biology , adherens junction , microbiology and biotechnology , psoriasis , cadherin , filaggrin , cancer research , immunology , tight junction , genetics , cell culture , cell , atopic dermatitis
Tumor Necrosis Factor‐α ( TNF ‐α) plays a pivotal role in psoriasis, an immuno‐mediated and genetic skin disease. Anti‐ TNF ‐α inhibitors, such as etanercept, are widely used in clinical practice. By immunofluorescence, we investigated the expression of junctional transmembrane proteins in desmosomes (desmocollin‐1, D sc1; desmoglein‐1, D sg1), adherens junctions ( E ‐cadherin), tight junctions (occludin), biomarkers of keratinocyte differentiation (keratin‐10, K 10; keratin‐14, K 14; keratin‐16, K 16; involucrin), epithelial proliferation and apoptosis in psoriatic skin before/after etanercept treatment ( n = 5) and in control skin samples ( n = 5). Occludin, K 14, K 16 and involucrin expressions were altered in psoriatic epidermis, while D sc1, D sg1, E ‐cadherin and K 10 localisations were comparable to controls. Etanercept promoted the restoration of the physiological condition as suggested by a more differentiated keratinocyte phenotype and a reduced epidermal proliferation rate.