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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >CD73-mediated adenosine production promotes stem cell-like properties in mouse Tc17 cells
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CD73-mediated adenosine production promotes stem cell-like properties in mouse Tc17 cells

机译：CD73介导的腺苷产生促进小鼠Tc17细胞的干细胞样特性

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The CD73 ectonucleotidase catalyses the hydrolysis of AMP to adenosine, an immunosuppressive molecule. Recent evidence has demonstrated that this ectonucleotidase is up-regulated in T helper type 17 cells when generated in the presence of transforming growth factor-beta (TGF-beta), and hence CD73 expression is related to the acquisition of immunosuppressive potential by these cells. TGF-beta is also able to induce CD73 expression in CD8(+) T cells but the function of this ectonucleotidase in CD8(+) T cells is still unknown. Here, we show that Tc17 cells present high levels of the CD73 ectonucleotidase and produce adenosine; however, they do not suppress the proliferation of CD4(+) T cells. Interestingly, we report that adenosine signalling through A2A receptor favours interleukin-17 production and the expression of stem cell-associated transcription factors such as tcf-7 and lef-1 but restrains the acquisition of Tc1-related effector molecules such as interferon-c and Granzyme B by Tc17 cells. Within the tumour microenvironment, CD73 is highly expressed in CD62L(+) CD127(+) CD8(+) T cells (memory T cells) and is down-regulated in GZMB(+) KLRG1(+) CD8(+) T cells (terminally differentiated T cells), demonstrating that CD73 is expressed in memoryaive cells and is down-regulated during differentiation. These data reveal a novel function of CD73 ectonucleotidase in arresting CD8(+) T-cell differentiation and support the idea that CD73-driven adenosine production by Tc17 cells may promote stem cell-like properties in Tc17 cells.
机译：CD73胞外核苷酸酶催化AMP水解为一种免疫抑制分子腺苷。最近的证据表明，当在转化生长因子-β（TGF-β）存在下产生时，这种胞外核苷酸酶在17型T辅助细胞中被上调，因此CD73的表达与这些细胞获得免疫抑制潜能有关。 TGF-β还能够诱导CD8（+）T细胞中的CD73表达，但是这种外切核苷酸酶在CD8（+）T细胞中的功能仍然未知。在这里，我们显示Tc17细胞呈现高水平的CD73胞外核苷酸酶并产生腺苷。但是，它们不能抑制CD4（+）T细胞的增殖。有趣的是，我们报道通过A2A受体的腺苷信号转导有利于白介素17的产生以及干细胞相关转录因子如tcf-7和lef-1的表达，但抑制了与Tc1相关的效应分子如干扰素c和cf的获得。 Tc17细胞产生的颗粒酶B。在肿瘤微环境内，CD73在CD62L（+）CD127（+）CD8（+）T细胞（记忆T细胞）中高表达，并在GZMB（+）KLRG1（+）CD8（+）T细胞中下调（ （最终分化的T细胞），表明CD73在记忆/幼稚细胞中表达，并在分化过程中被下调。这些数据揭示了CD73胞外核苷酸酶在阻止CD8（+）T细胞分化中的新功能，并支持Tc17细胞CD73驱动的腺苷生产可能促进Tc17细胞中干细胞样特性的想法。

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