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Analysis of anti-TNF-induced skin lesions reveals strong Th1 activation with some distinct immunological characteristics.

Analysis of anti-TNF-induced skin lesions reveals strong Th1 activation with some distinct immunological characteristics.
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Stoffel E, Maier H, Riedl E, Brüggen MC, Reininger B, Schaschinger M, Bangert C, Guenova E, Stingl G, Brunner PM,


Stoffel E, Maier H, Riedl E, Brüggen MC, Reininger B, Schaschinger M, Bangert C, Guenova E, Stingl G, Brunner PM, (click to view)

Stoffel E, Maier H, Riedl E, Brüggen MC, Reininger B, Schaschinger M, Bangert C, Guenova E, Stingl G, Brunner PM,

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The British journal of dermatology 2017 11 16() doi 10.1111/bjd.16126
Abstract
BACKGROUND
Psoriasiform and eczematous eruptions are the most common dermatological adverse reaction linked to anti-TNF-α therapy. Yet, a detailed characterization of their immune phenotype is lacking.

OBJECTIVES
We sought to characterize anti-TNF-α induced inflammatory skin lesions on a histopathologic, cellular and molecular level, compared to psoriasis, eczema (atopic dermatitis), and healthy control skin.

METHODS
Histopathologic evaluation, gene expression (quantitative RT-PCR) and computer-assisted immunohistologic studies (TissueFAXS) were performed on 19 skin biopsies from IBD (n=17) and rheumatoid arthritis (n=2) patients with new-onset inflammatory skin lesions during anti-TNF-α-therapy.

RESULTS
While most biopsies showed a psoriasiform and/or spongiotic (eczematous) histopathologic architecture, these lesions were inconsistent with either psoriasis or eczema on a molecular level using an established CCL27/iNOS classifier. Despite some differences in immune skewing depending on the specific histopathologic reaction pattern, all anti-TNF-α-induced lesions showed strong IFN-γ activation, at higher levels than in psoriasis or eczema. IFN-γ was most likely produced by CD3/CD4/Tbet-positive Th1 lymphocytes.

CONCLUSIONS
New-onset anti-TNF-α-induced eruptions previously classified as psoriasis or spongiotic dermatitis (eczema) exhibit a molecular profile that is different from either of these disorders. This article is protected by copyright. All rights reserved.

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