Unit of Immunotoxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
J Invest Dermatol. 2012 Jun;132(6):1672-80. doi: 10.1038/jid.2012.40. Epub 2012 Mar 8.
The role of Foxp3+ regulatory T (Treg) cells in atopic dermatitis (AD) is still unclear. In a murine AD model, the number of Foxp3+ cells increased in the allergen-exposed skin area and in the secondary lymphoid organs. Both Foxp3+ and Foxp3- IL-10+ T cells accumulated at the site of allergen exposure, and CD103+ effector/memory Foxp3+ Treg cells expanded gradually in the lymph nodes throughout the sensitization protocol. The depletion of Foxp3+ Treg cells led to significantly exacerbated skin inflammation, including increased recruitment of inflammatory cells and expression of T helper type 2 cytokines, as well as elevated serum IgE levels. The effect of depleting Treg cells during epicutaneous sensitization was mirrored off by a stronger inflammatory response also in the lungs following airway challenge. Thus, Treg cells have an important role in controlling AD-like inflammation and the transfer of allergic skin inflammation to the lungs.
Foxp3+ 调节性 T(Treg)细胞在特应性皮炎(AD)中的作用尚不清楚。在小鼠 AD 模型中,过敏原暴露皮肤区域和次级淋巴器官中的 Foxp3+细胞数量增加。Foxp3+ 和 Foxp3-IL-10+T 细胞在过敏原暴露部位聚集,CD103+效应/记忆 Foxp3+Treg 细胞在整个致敏方案中逐渐在淋巴结中扩增。Foxp3+Treg 细胞耗竭导致皮肤炎症明显加重,包括炎症细胞募集增加和 T 辅助细胞 2 型细胞因子表达增加,以及血清 IgE 水平升高。在经皮致敏期间耗尽 Treg 细胞的作用,在气道挑战后肺部也出现更强的炎症反应中得到体现。因此,Treg 细胞在控制 AD 样炎症和将过敏性皮肤炎症转移到肺部方面具有重要作用。