Department of Experimental and Clinical Medicine and DENOTHE Center, University of Florence, Florence, Italy.
Eur J Immunol. 2017 Apr;47(4):633-636. doi: 10.1002/eji.201746986.
Granulomatosis with Polyangiitis (GPA) (formerly known as Wegener's granulomatosis) is a vasculitis of unknown etiology affecting predominantly small- to medium-sized vessels, usually involving the upper and lower respiratory tract and kidneys. Anti-neutrophil cytoplasmic autoantibodies are probably the initial cause of the inflammatory process that leads to the typical necrotizing lesions. In this issue of the European Journal of Immunology, Szczeklik et al. [Eur. J. Immunol. 2017. 47: 724-733] report some interesting findings on the possible involvement of T-cell subsets in the pathogenesis of the disease. This prospective study, performed on a large cohort of patients, identifies Th17 lymphocytes as the possible pathogenic subset of GPA, and Treg cells as the possible suppressors of the inflammatory process. These two subsets in peripheral blood could be used as cellular biomarkers of disease activity, and this would result particularly useful in the follow-up of patients once the immunosuppressive treatment has been initiated.
肉芽肿性多血管炎（GPA）（以前称为韦格纳肉芽肿病）是一种病因不明的血管炎，主要影响中小血管，通常累及上呼吸道和下呼吸道及肾脏。抗中性粒细胞胞质自身抗体可能是导致典型坏死性病变的炎症过程的最初原因。在本期《欧洲免疫学杂志》中，Szczeklik 等人[Eur. J. Immunol. 2017. 47: 724-733]报告了关于 T 细胞亚群在疾病发病机制中可能的参与的一些有趣发现。这项前瞻性研究对一大群患者进行了研究，确定了 Th17 淋巴细胞是 GPA 的可能致病性亚群，而 Treg 细胞是炎症过程的可能抑制物。这两个外周血中的亚群可以作为疾病活动的细胞生物标志物，这在开始免疫抑制治疗后对患者的随访尤其有用。
