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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >IL-12 reverses anergy to T cell receptor triggering in human lung tumor-associated memory T cells.
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IL-12 reverses anergy to T cell receptor triggering in human lung tumor-associated memory T cells.

机译：IL-12逆转人类肺部肿瘤相关记忆T细胞中T细胞受体触发的无反应。

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Memory T cells in human non-small cell lung cancer are unresponsive to progressing tumors. T cells were evaluated at the single cell level by imaging the nuclear translocation of NF-kappaB and NFAT via immunofluorescence confocal microscopy as an early measure of responsiveness to T cell receptor triggering. Little translocation of NF-kappaB or NFAT occurred in tumor-associated T cells in response to CD3+CD28 cross-linking under conditions which led to maximal translocation in normal donor peripheral blood T cells. TNF-alpha induced maximal NF-kappaB translocation in these T cells, indicating that they remain receptive to alternative signaling pathways, and pulsing with IL-12 prior to TCR triggering reversed their apparent anergy. T cells from additional chronic inflammatory microenvironments demonstrated a similar refractoriness to TCR activation, suggesting either that a common regulatory mechanism present within the microenvironment controls these cells or that with continuous antigen exposure, theyremain refractory to activation via the TCR.
机译：人类非小细胞肺癌中的记忆T细胞对进展中的肿瘤无反应。通过免疫荧光共聚焦显微镜对NF-kappaB和NFAT的核易位进行成像来评估T细胞在单细胞水平上的作用，以此作为对T细胞受体触发反应的早期测量。在导致正常供体外周血T细胞最大移位的条件下，响应于CD3 + CD28交联的肿瘤相关T细胞中几乎没有NF-κB或NFAT移位。 TNF-α在这些T细胞中诱导了最大的NF-κB易位，表明它们仍能接受其他信号途径，并且在TCR触发之前用IL-12脉冲逆转了它们的明显无能。来自其他慢性炎症性微环境的T细胞表现出与TCR激活相似的难治性，这表明存在于微环境中的常见调节机制控制着这些细胞，或者持续不断的抗原暴露，使得它们对通过TCR的激活保持顽固性。

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