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Molecular programming of steady-state dendritic cells: impact on autoimmunity and tumor immune surveillance

机译：稳态树突细胞的分子规划：对自身免疫和肿瘤免疫监测的影响

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Dendritic cells are master regulators of immunity. Immature dendritic cells are essential for maintaining selftolerance, while mature dendritic cells initiate a variety of specialized immune responses. Dendritic cell quiescence is often viewed as a default state that requires exogenous stimuli to induce maturation. However, recent studies have identified dendritic cell quiescence factors that actively program dendritic cells to an immature state. In the absence of these factors, dendritic cells spontaneously become immunogenic and can induce autoimmune responses. Herein we discuss two such factors, NF-κB1 and A20, that preserve dendritic cell immaturity through their regulation of NF-κB signaling. Loss of either of these factors increases dendritic cell immunogenicity, suggesting that they may be important targets for enhancing dendritic cell–based cancer immunotherapies. Alternatively, defects in molecules critical for maintaining steady-state DCs may provide novel biomarkers that identify patients who have enhanced natural antitumor immunity or that correlate with better responses to various immunotherapies.
机译：树突细胞是免疫的主调节器。未成熟的树突状细胞是维持selftolerance必不可少的，而成熟树突状细胞发起各种专门的免疫反应。树突状细胞静止通常被视为需要外源性刺激，以诱导成熟一个默认状态。然而，最近的研究已经确定了树突状细胞静息因素的积极方案树突状细胞的不成熟状态。在不存在这些因素，树突细胞自发地成为免疫原性的，并且可以诱导自身免疫应答。在这里我们将讨论两个这样的因素，NF-κB1和A20，通过他们的NF-κB信号通路的调节保护树突状细胞的不成熟。任这些因素流失扩大树突状细胞的免疫原性，这表明它们可能是重要的目标，加强树突状细胞癌症免疫。或者，在用于维持稳态的DC可以提供确定患者谁具有增强的天然抗肿瘤免疫力或与各种免疫疗法更好的反应相关成分的该生物标志物的新关键分子的缺陷。

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