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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Macrophages play an essential role in antigen-specific immune suppression mediated by T CD8(+) cell-derived exosomes
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Macrophages play an essential role in antigen-specific immune suppression mediated by T CD8(+) cell-derived exosomes

机译：巨噬细胞在T CD8（+）细胞源性外来体介导的抗原特异性免疫抑制中起重要作用

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摘要

Murine contact sensitivity (CS) reaction could be antigen-specifically regulated by T CD8(+) suppressor (Ts) lymphocytes releasing microRNA-150 in antibody light-chain-coated exosomes that were formerly suggested to suppress CS through action on macrophages (M phi). The present studies investigated the role of M phi in Ts cell-exosome-mediated antigen-specific suppression as well as modulation of M phi antigen-presenting function in humoral and cellular immunity by suppressive exosomes. Mice depleted of M phi by clodronate liposomes could not be tolerized and did not produce suppressive exosomes. Moreover, isolated T effector lymphocytes transferring CS were suppressed by exosomes only in the presence of M phi, demonstrating the substantial role of M phi in the generation and action of Ts cell regulatory exosomes. Further, significant decrease of number of splenic B cells producing trinitrophenyl (TNP) -specific antibodies with the alteration of the ratio of serum titres of IgM to IgG was observed in recipients of exosome-treated, antigen-pulsed M phi and the significant suppression of CS was demonstrated in recipients of exosome-treated, TNP-conjugated M phi. Additionally, exosome-pulsed, TNP-conjugated M phi mediated suppression of CS in mice pre-treated with a low-dose of cyclophosphamide, suggesting de novo induction of T regulatory (Treg) lymphocytes. Treg cell involvement in the effector phase of the studied suppression mechanism was proved by unsuccessful tolerization of DEREG mice depleted of Treg lymphocytes. Furthermore, the inhibition of proliferation of CS effector cells cultured with exosome-treated M phi in a transmembrane manner was observed. Our results demonstrated the essential role of M phi in antigen-specific immune suppression mediated by Ts cell-derived exosomes and realized by induction of Treg lymphocytes and inhibition of T effector cell proliferation.
机译：鼠接触敏感性（CS）反应可能受T CD8（+）抑制（Ts）淋巴细胞的抗原特异性调节，该淋巴细胞在抗体轻链包裹的外泌体中释放microRNA-150，以前建议通过对巨噬细胞（M phi）的作用来抑制CS ）。本研究调查了M phi在Ts细胞外来体介导的抗原特异性抑制中的作用以及抑制性外泌体在体液和细胞免疫中对M phi抗原呈递功能的调节。氯膦酸盐脂质体耗尽M phi的小鼠不能耐受，也不产生抑制性外泌体。此外，仅在M phi存在的情况下，外泌体才抑制转移CS的分离的T效应淋巴细胞，证明M phi在Ts细胞调节性外泌体的产生和作用中的重要作用。此外，在接受外体处理的，经抗原脉冲刺激的M phi受体中观察到了产生三硝基苯基（TNP）特异性抗体的脾脏B细胞数量的显着减少，其中IgM与IgG的血清滴度之比发生了变化，并且显着抑制了CS在外泌体处理的TNP缀合的M phi的受体中得到证实。此外，在低剂量环磷酰胺预处理的小鼠中，外泌体脉冲，TNP偶联的M phi介导的CS抑制，提示从头诱导T调节（Treg）淋巴细胞。 Treg细胞参与了研究的抑制机制的效应期，这是由于对TREG淋巴细胞耗竭的DEREG小鼠耐受性不佳所致。此外，观察到以外膜方式抑制用外来体处理的M phi培养的CS效应细胞的增殖。我们的结果证明了M phi在由Ts细胞衍生的外来体介导的抗原特异性免疫抑制中的重要作用，并通过诱导Treg淋巴细胞和抑制T效应细胞增殖而实现。

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