Infection and cancer suppress pDC derived IFN-I.
Infection and cancer suppress pDC derived IFN-I.
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DOI：
10.1016/j.coi.2020.08.001
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发表时间：
2020-10
影响因子：
7
通讯作者：
Zuniga EI
中科院分区：
文献类型：
--
作者：
Greene TT;Jo YR;Zuniga EI
浆细胞样树突状细胞（pDC）是促进抗病毒和抗肿瘤免疫的I型干扰素（IFN-I）的专门生产者。然而，慢性感染和癌症抑制pDC衍生的IFN-I。虽然这种抑制的机制多种多样，但它们可以大致分为两类：i）pDC IFN-1产生能力的降低或消除（功能耗竭）和/或ii）pDC数量的减少（改变的群体动力学）。最近的工作已经确定了在慢性感染和癌症期间有助于抑制pDC衍生的IFN-I的许多过程，包括通过Toll样受体（TLR）的持续刺激、抑制性微环境、抑制性受体连接以及骨髓祖细胞和细胞凋亡的发育减少。在通过TLR活化治疗疾病中利用pDC的新兴成功说明了靶向pDC的治疗潜力。对限制pDC衍生的IFN-I的系统的更深入理解具有改善这些新兴疗法的潜力，并且有助于设计利用pDC的突出IFN-I生产能力的新方法。
Plasmacytoid dendritic cells (pDCs) are specialized producers of Type I interferon (IFN-I) that promote anti-viral and anti-tumor immunity. However, chronic infections and cancer inhibit pDC-derived IFN-I. While the mechanisms of this inhibition are multifarious they can be classified broadly into two categories: i) reduction or ablation of pDC IFN-I-production capacity (functional exhaustion) and/or ii) decrease in pDC numbers (altered population dynamics). Recent work has identified many processes that contribute to suppression of pDC-derived IFN-I during chronic infections and cancer, including sustained stimulation through Toll Like Receptors (TLRs), inhibitory microenvironments, inhibitory receptor ligation, and reduced development from bone marrow progenitors and apoptosis. Emerging success leveraging pDCs in treatment of disease through TLR activation illustrates the therapeutic potential of targeting pDCs. Deeper understanding of the systems that limit pDC-derived IFN-I has the potential to improve these emerging therapies as well as help devising new approaches that harness the outstanding IFN-I-production capacity of pDCs.
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