Inflammation, Chimiokines et Immunopathologie, INSERM UMR996, University Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.
Allergy Research Group, Department of Dermatology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Front Immunol. 2019 May 7;10:1004. doi: 10.3389/fimmu.2019.01004. eCollection 2019.
Exposure to certain chemicals disturbs skin homeostasis. In particular, protein-reactive chemical contact sensitizers trigger an inflammatory immune response resulting in eczema and allergic contact dermatitis. Chemical sensitizers activate innate immune cells which orchestrate the skin immune response. This involves oxidative and inflammatory pathways. In parallel, the Nrf2/Keap1 pathway, a major ubiquitous regulator of cellular oxidative and electrophilic stress is activated in the different skin innate immune cells including epidermal Langerhans cells and dermal dendritic cells, but also in keratinocytes. In this context, Nrf2 shows a strong protective capacity through the downregulation of both the oxidative stress and inflammatory pathways. In this review we highlight the important role of Nrf2 in the control of the innate immune response of the skin to chemical sensitizers.
接触某些化学物质会扰乱皮肤的内稳态。特别是，蛋白反应性化学接触致敏原会引发炎症免疫反应，导致湿疹和过敏性接触性皮炎。化学致敏原激活先天免疫细胞，从而协调皮肤免疫反应。这涉及氧化和炎症途径。与此同时，Nrf2/Keap1 通路作为细胞氧化和亲电应激的主要普遍调节剂，在不同的皮肤先天免疫细胞中被激活，包括表皮朗格汉斯细胞和真皮树突状细胞，也包括角质形成细胞。在这种情况下，Nrf2 通过下调氧化应激和炎症途径显示出强大的保护能力。在这篇综述中，我们强调了 Nrf2 在控制皮肤对化学致敏原的先天免疫反应中的重要作用。
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