Figure 1: Cytokine-expression profiles after activation of PRRs.

在病毒感染过程中，产生干扰素（抗病毒应答的一种主要介体）所需要的相关免疫通路的激活会抑制一种对抵抗细菌感染有重要作用的细胞因子IL-12的产生，这是日前出版的《自然—免疫学》Nature Immunology上一项研究得出的结论。

一些受体可针对入侵的病原体激活相应的免疫介体。由这些受体激活的信号通路可通过数种方式相互作用，包括协作、互补、代偿等。Tadatsugu Taniguchi等人观察到在抗病毒应答过程中，一种经过诱导生成的产生干扰素所必需的转录因子IRF3，能直接抑制编码IL-12的基因的转录。

除此之外，他们还注意到，就算小鼠体内的细菌数并未达到致死量，病毒感染仍然会通过减弱小鼠的抗菌应答而导致小鼠死亡率上升。这种干扰作用可能有利于保护宿主在抗病毒应答中不产生过多炎症，却会在由多种病菌造成的多重感染中产生消极作用。

Cross-interference of RLR and TLR signaling pathways modulates antibacterial T cell responses

Although the mechanisms by which innate pathogen-recognition receptors enhance adaptive immune responses are increasingly well understood, whether signaling events from distinct classes of receptors affect each other in modulating adaptive immunity remains unclear. We found here that the activation of cytosolic RIG-I-like receptors （RLRs） resulted in the selective suppression of transcription of the gene encoding the p40 subunit of interleukin 12 （Il12b） that was effectively induced by the activation of Toll-like receptors （TLRs）. The RLR-activated transcription factor IRF3 bound dominantly, relative to IRF5, to the Il12b promoter, where it interfered with the TLR-induced assembly of a productive transcription-factor complex. The activation of RLRs in mice attenuated TLR-induced responses of the T helper type 1 cell （TH1 cell） and interleukin 17–producing helper T cell （TH17 cell） subset types and, consequently, viral infection of mice caused death at sublethal doses of bacterial infection. The innate immune receptor cross-interference we describe may have implications for infection-associated clinical episodes.