Department of Immunology, Institut Curie, Paris, France; Laboratory of Neuroimmunology, Fondazione Santa Lucia, Rome, Italy.
Department of Immunology, Institut Curie, Paris, France; Institut National de la Santé et de la Recherche Médicale U932, Paris, France; Research Section, Institut Curie, Paris, France.
J Allergy Clin Immunol. 2014 Aug;134(2):373-81. doi: 10.1016/j.jaci.2014.04.022. Epub 2014 Jun 6.
Thymic stromal lymphopoietin (TSLP) is a major proallergic cytokine that promotes TH2 responses through dendritic cell (DC) activation. Whether it also plays a role in human autoimmune inflammation and associated pathways is not known.
In this study we investigated the potential role of several epithelium-derived factors, including TSLP, in inducing IL-23 production by human DCs. We further dissected the role of TSLP in patients with psoriasis, an IL-23-associated skin autoimmune disease.
The study was performed in human subjects using primary cells and tissue samples from patients with psoriasis and healthy donors. We analyzed the production of IL-23 in vitro by blood and skin DCs. We studied the function for TSLP and its interaction with other components of the inflammatory microenvironment in situ and ex vivo.
We found that TSLP synergized with CD40 ligand to promote DC activation and pathogenic IL-23 production by primary blood and skin DCs. In situ TSLP was strongly expressed by keratinocytes of untreated psoriatic lesions but not in normal skin. Moreover, we could demonstrate that IL-4, an important component of the TH2 inflammation seen in patients with atopic dermatitis, inhibited IL-23 production induced by TSLP and CD40 ligand in a signal transducer and activator of transcription 6-independent manner.
Our results identify TSLP as a novel player within the complex psoriasis cytokine network. Blocking TSLP in patients with psoriasis might contribute to decreasing DC activation and shutting down the production of pathogenic IL-23.
胸腺基质淋巴细胞生成素(TSLP)是一种主要的促过敏细胞因子,通过树突状细胞(DC)的激活促进 TH2 反应。目前尚不清楚它是否在人类自身免疫炎症及其相关途径中发挥作用。
本研究旨在探讨几种上皮来源的因子(包括 TSLP)在诱导人 DC 产生 IL-23 中的潜在作用。我们进一步研究了 TSLP 在银屑病患者中的作用,银屑病是一种与 IL-23 相关的皮肤自身免疫性疾病。
本研究采用原代细胞和银屑病患者及健康供体的组织样本,在人体受试者中进行。我们分析了血液和皮肤 DC 体外产生的 IL-23。我们研究了 TSLP 的功能及其与炎症微环境中其他成分的相互作用。
我们发现 TSLP 与 CD40 配体协同作用,促进原代血液和皮肤 DC 的激活和致病性 IL-23 的产生。未经治疗的银屑病皮损角质形成细胞中强烈表达 TSLP,但在正常皮肤中不表达。此外,我们可以证明,TH2 炎症的重要组成部分——白细胞介素-4(IL-4),以信号转导和转录激活因子 6 非依赖性方式抑制 TSLP 和 CD40 配体诱导的 IL-23 产生。
我们的研究结果表明,TSLP 是复杂的银屑病细胞因子网络中的一个新成员。在银屑病患者中阻断 TSLP 可能有助于减少 DC 激活和阻断致病性 IL-23 的产生。