Human lung transplant recipients undergoing rejection induce circulatory exosomes with lung self-antigens (SAgs), K-alpha 1 Tubulin and Collagen V, and immunization of C57BL/6 mice with exosomes induced obliterative airway disease (HEI-OAD). We analyzed whether exosomes with SAgs induced immunity in microRNA-155 knockout mice (miR-155KO), as microRNA-155 is an immune regulator. C57BL/6 and miR-155KO were immunized with exosomes from stable or chronic rejection (bronchiolitis obliterans syndrome (BOS) and on day 30, induction of exosomes, antibodies (Abs) to SAgs and cellular immunity were determined. C57BL/6 immunized with exosomes from BOS developed OAD. These immunized animals also developed Abs to SAgs and increased frequency of SAg-specific IFNγ and IL17- producing cells. In contrast, Abs to SAgs did not develop in miR-155KO and there was reduction in frequency of cells producing IL10. Upregulation of suppressor of cytokine signaling for lung inflammation was also noted resulting in abrogation of induction of exosomes with SAgs OAD.

接受排斥的人肺移植受者诱导循环外泌体产生肺自身抗原 (SAg)、K-α 1 微管蛋白和胶原 V，并用外泌体免疫 C57BL/6 小鼠诱导闭塞性气道疾病 (HEI-OAD)。我们分析了具有 SAg 的外泌体是否在 microRNA-155 敲除小鼠 (miR-155KO) 中诱导免疫，因为 microRNA-155 是一种免疫调节剂。C57BL/6 和 miR-155KO 用来自稳定或慢性排斥反应（闭塞性细支气管炎综合征 (BOS) 的外泌体进行免疫），在第 30 天，确定外泌体的诱导、SAg 抗体（Abs）和细胞免疫。用外泌体免疫 C57BL/6来自 BOS 的 BOS 产生了 OAD。这些免疫的动物也产生了对 SAg 的抗体，并增加了 SAg 特异性 IFNγ 和 IL17 产生细胞的频率。相反，在 miR-155KO 中未出现针对 SAg 的抗体，并且产生 IL10 的细胞频率降低。还注意到肺部炎症的细胞因子信号抑制因子的上调，导致外泌体与 SAg OAD 的诱导被废除。