Type III IFNs Are Commonly Induced by Bacteria-Sensing TLRs and Reinforce Epithelial Barriers during Infection.
Type III IFNs Are Commonly Induced by Bacteria-Sensing TLRs and Reinforce Epithelial Barriers during Infection.
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DOI：
10.4049/jimmunol.1700250
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发表时间：
2017-11-01
期刊：
影响因子：
--
通讯作者：
Kagan JC
中科院分区：
文献类型：
--
作者：
Odendall C;Voak AA;Kagan JC
III型干扰素（IFNλs）是一种分泌因子，因其抗病毒活性而闻名。然而，它们在细菌感染期间的调节和功能尚不清楚。在此，我们报道了IFNλ基因的调节与Toll样受体（TLR）控制I型IFN表达的机制无关。虽然I型IFN仅从存在于核内体上的TLR表达，但III型IFN可由存在于质膜上并检测各种细菌产物的TLR诱导。调节III型IFN基因表达的机制与促进炎性细胞因子和趋化因子表达的机制相同。重要的是，重组IFNλs在体外增强上皮屏障，防止跨细胞细菌传播。因此，我们建议，除了他们的功能，在细胞内在的抗病毒免疫，III型干扰素保护上皮屏障的完整性，活动，将有利于主机在任何感染的遭遇。
Type III interferons (IFNλs) are secreted factors that are well-known for their antiviral activities. However, their regulation and functions during bacterial infections are unclear. Herein, we report that the regulation of IFNλ genes did not track with mechanisms that control type I IFN expression in response to Toll-like Receptors (TLRs). While type I IFNs were only expressed from TLRs present on endosomes, type III IFNs could be induced by TLRs that reside at the plasma membrane and that detect various bacterial products. The mechanisms that regulate type III IFN gene expression tracked with those that promote inflammatory cytokine and chemokine expression. Importantly, recombinant IFNλs enhanced epithelial barriers in vitro, preventing transcellular bacteria dissemination. We therefore propose that in addition to their functions in cell-intrinsic antiviral immunity, type III IFNs protect epithelial barrier integrity, an activity that would benefit the host during any infectious encounter.
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