Institut für Experimentelle Immunologie und Hepatologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
J Am Soc Nephrol. 2013 May;24(6):930-42. doi: 10.1681/ASN.2012070684. Epub 2013 May 2.
Regulatory T cells (Tregs) exert their immunosuppressive activity through several immunoregulatory mechanisms, including the production of anti-inflammatory cytokines such as IL-10. Although several studies suggest a role for Tregs in modulating crescentic GN, the underlying mechanisms are not well understood. Here, using IL-10 reporter mice, we detected IL-10-producing Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic GN. Specific inactivation of Il10 in Foxp3(+) Tregs eliminated the ability of these cells to suppress renal and systemic production of IFNγ and IL-17; these IL-10-deficient Tregs lost their capacity to attenuate renal tissue injury. These data highlight the suppressive functions of Tregs in crescentic GN and suggest the importance of Treg-derived IL-10 in ameliorating disease severity and in modulating both the Th1 and most notably Th17 immune response.
调节性 T 细胞（Tregs）通过几种免疫调节机制发挥其免疫抑制活性，包括产生抗炎细胞因子，如 IL-10。尽管有几项研究表明 Tregs 在调节新月体肾炎中起作用，但潜在机制尚不清楚。在这里，我们使用 IL-10 报告小鼠，在新月体肾炎的小鼠模型中检测到肾脏、血液和次级淋巴组织中产生 IL-10 的 Foxp3(+) T 细胞。Foxp3(+) Tregs 中特异性失活 Il10 消除了这些细胞抑制肾脏和全身 IFNγ 和 IL-17 产生的能力；这些缺乏 IL-10 的 Tregs 失去了减轻肾组织损伤的能力。这些数据突出了 Tregs 在新月体肾炎中的抑制功能，并表明 Treg 衍生的 IL-10 在改善疾病严重程度以及调节 Th1 和特别是 Th17 免疫反应方面的重要性。
