Department of Immunology, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Division of Pediatric Pneumology & Allergology, University Medical Center Schleswig-Holstein, 23538, Lübeck, Germany.
Nat Commun. 2021 Oct 8;12(1):5911. doi: 10.1038/s41467-021-26134-w.
Immune cells at sites of inflammation are continuously activated by local antigens and cytokines, and regulatory mechanisms must be enacted to control inflammation. The stepwise hydrolysis of extracellular ATP by ectonucleotidases CD39 and CD73 generates adenosine, a potent immune suppressor. Here we report that human effector CD8 T cells contribute to adenosine production by releasing CD73-containing extracellular vesicles upon activation. These extracellular vesicles have AMPase activity, and the resulting adenosine mediates immune suppression independently of regulatory T cells. In addition, we show that extracellular vesicles isolated from the synovial fluid of patients with juvenile idiopathic arthritis contribute to T cell suppression in a CD73-dependent manner. Our results suggest that the generation of adenosine upon T cell activation is an intrinsic mechanism of human effector T cells that complements regulatory T cell-mediated suppression in the inflamed tissue. Finally, our data underscore the role of immune cell-derived extracellular vesicles in the control of immune responses.
炎症部位的免疫细胞不断受到局部抗原和细胞因子的激活,必须采取调节机制来控制炎症。细胞外核苷酸酶 CD39 和 CD73 逐步水解细胞外 ATP 生成腺苷,这是一种有效的免疫抑制剂。本研究报道人类效应 CD8 T 细胞在激活时通过释放含有 CD73 的细胞外囊泡参与腺苷生成。这些细胞外囊泡具有 AMP 酶活性,产生的腺苷通过独立于调节性 T 细胞的机制介导免疫抑制。此外,本研究还表明,从小儿特发性关节炎患者的滑液中分离的细胞外囊泡以 CD73 依赖的方式有助于 T 细胞抑制。这些结果表明,T 细胞激活时产生的腺苷是人类效应 T 细胞的内在机制,补充了炎症组织中调节性 T 细胞介导的抑制作用。最后,本研究数据强调了免疫细胞来源的细胞外囊泡在控制免疫反应中的作用。