Department of Dermatology, Division of Immunology, Allergy and Infectious Diseases, Medical University of Vienna, Vienna, Austria.
Faculty of Medicine, University of Zurich, Zurich, Switzerland.
Br J Dermatol. 2018 May;178(5):1151-1162. doi: 10.1111/bjd.16126. Epub 2018 Mar 6.
Psoriasiform and eczematous eruptions are the most common dermatological adverse reactions linked to anti-tumour necrosis factor (TNF)-α therapy. Yet, a detailed characterization of their immune phenotype is lacking.
To characterize anti-TNF-α-induced inflammatory skin lesions at a histopathological, cellular and molecular level, compared with psoriasis, eczema (atopic dermatitis) and healthy control skin.
Histopathological evaluation, gene expression (quantitative real-time polymerase chain reaction) and computer-assisted immunohistological studies (TissueFAXS) were performed on 19 skin biopsies from patients with inflammatory bowel disease (n = 17) and rheumatoid arthritis (n = 2) with new-onset inflammatory skin lesions during anti-TNF-α-therapy.
Although most biopsies showed a psoriasiform and/or spongiotic (eczematous) histopathological architecture, these lesions were inconsistent with either psoriasis or eczema on a molecular level using an established chemokine (C-C motif) ligand 27/inducible nitric oxide synthase classifier. Despite some differences in immune skewing depending on the specific histopathological reaction pattern, all anti-TNF-α-induced lesions showed strong interferon (IFN)-γ activation, at higher levels than in psoriasis or eczema. IFN-γ was most likely produced by CD3/CD4/Tbet-positive T helper 1 lymphocytes.
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.
类银屑病样和湿疹样皮疹是与抗肿瘤坏死因子（TNF）-α 治疗相关的最常见皮肤不良反应。然而，它们的免疫表型特征尚不清楚。
在组织病理学、细胞和分子水平上，比较抗 TNF-α 诱导的炎症性皮肤病变与银屑病、湿疹（特应性皮炎）和健康对照皮肤，以确定其特征。
对 19 例炎症性肠病（n=17）和类风湿关节炎（n=2）患者在接受抗 TNF-α 治疗期间新出现炎症性皮肤病变的皮肤活检标本进行组织病理学评估、基因表达（实时定量聚合酶链反应）和计算机辅助免疫组织化学研究（TissueFAXS）。
尽管大多数活检显示类银屑病样和/或海绵状（湿疹样）组织病理学结构，但这些病变在分子水平上与银屑病或湿疹均不一致，使用已建立的趋化因子（C-C 基序）配体 27/诱导型一氧化氮合酶分类器。尽管根据特定的组织病理学反应模式存在一些免疫偏向差异，但所有抗 TNF-α 诱导的病变均显示强烈的干扰素（IFN）-γ激活，其水平高于银屑病或湿疹。IFN-γ很可能是由 CD3/CD4/Tbet 阳性辅助性 T 淋巴细胞产生的。
先前分类为银屑病或海绵状性皮炎（湿疹）的新出现的抗 TNF-α 诱导性皮疹表现出与这两种疾病均不同的分子谱。
