Garzorz N, Alsisi M, Todorova A, Atenhan A, Thomas J, Lauffer F, Ring J, Schmidt-Weber C, Biedermann T, Eyerich S, Eyerich K
Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.
ZAUM - Center of Allergy and Environment, Technical University of Munich and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
J Eur Acad Dermatol Venereol. 2015 Dec;29(12):2429-35. doi: 10.1111/jdv.13325. Epub 2015 Sep 28.
Alopecia areata (AA) is a T-cell-driven autoimmune disease of the hair follicle and frequently reported to be associated with inflammatory skin diseases (ISD) such as atopic eczema (AE) or psoriasis. Interestingly, AA on the one hand and both AE and psoriasis on the other hand are believed to be driven by mutually antagonistic T-cell subsets.
To characterize AA-specific T-cell profiles and inflammatory pattern by intra-individual comparison of AA and coexistent ISD.
112 patients with AA were recruited and investigated for coexisting ISD. In-depth analyses were performed in patients with AA and AE (n = 2), AA and psoriasis (n = 1), AA and psoriasis and AE (n = 1) and AA and lichen planus (n = 1), using histology, immunohistochemistry and cytokine staining of T cells isolated from lesional skin.
Of 112 AA patients investigated, 23 suffered from an ISD. The prevalence of AE, vitiligo, psoriasis and lichen planus was higher in the investigated AA cohort than in the normal population. The clinical as well as histological phenotype of AA the coexistent ISD were unequivocal. In line with this, T-cell infiltrates were found to be disease-characteristics with AA and lichen planus dominated by CD8+ and IFN-γ+ TNF-α+ producing T cells while psoriasis lesions in the same patients were dominated by IL-17+ and AE by IL-4+ T cells.
AA patients have a higher incidence of various T-cell-driven inflammatory skin diseases than the normal population, a phenomenon which might relate to over-activation of skin-homing T cells and to specific immune triggers as the primary cause of inflammation. More importantly, we showed that by using AA as a model disease, our approach of intra-individual comparison of distinct inflammatory responses in the same patient is feasible and offers the unique possibility to gain insights into disease pathogenesis independent from genetic susceptibilities.
斑秃（AA）是一种由T细胞驱动的毛囊自身免疫性疾病，常被报道与炎症性皮肤病（ISD）相关，如特应性皮炎（AE）或银屑病。有趣的是，一方面斑秃，另一方面特应性皮炎和银屑病，被认为是由相互拮抗的T细胞亚群驱动的。
通过对斑秃及共存的炎症性皮肤病进行个体内比较，以表征斑秃特异性T细胞谱和炎症模式。
招募112例斑秃患者，并对其共存的炎症性皮肤病进行调查。对患有斑秃合并特应性皮炎（n = 2）、斑秃合并银屑病（n = 1）、斑秃合并银屑病和特应性皮炎（n = 1）以及斑秃合并扁平苔藓（n = 1）的患者进行深入分析，采用组织学、免疫组织化学以及对从皮损处分离的T细胞进行细胞因子染色的方法。
在接受调查的112例斑秃患者中，23例患有炎症性皮肤病。在被调查的斑秃队列中，特应性皮炎、白癜风、银屑病和扁平苔藓的患病率高于正常人群。斑秃及共存的炎症性皮肤病的临床及组织学表型明确。与此一致的是，发现T细胞浸润具有疾病特征，斑秃和扁平苔藓以产生CD8+和IFN-γ+TNF-α+的T细胞为主，而同一患者的银屑病皮损以IL-17+T细胞为主，特应性皮炎以IL-4+T细胞为主。
斑秃患者发生各种由T细胞驱动的炎症性皮肤病的发生率高于正常人群，这一现象可能与归巢至皮肤的T细胞过度活化以及特定的免疫触发因素作为炎症的主要原因有关。更重要的是，我们表明，以斑秃作为模型疾病，我们在同一患者中对不同炎症反应进行个体内比较的方法是可行的，并且提供了独立于遗传易感性深入了解疾病发病机制的独特可能性。
