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

在病毒感染過程中，產生干擾素（抗病毒應答的一種主要介體）所需要的相關免疫通路的激活會抑制一種對抵抗細菌感染有重要作用的細胞因子IL-12的產生，這是日前出版的《自然—免疫學》Nature Immunology上一項研究得出的結論。

一些受體可針對入侵的病原體激活相應的免疫介體。由這些受體激活的信號通路可通過數種方式相互作用，包括協作、互補、代償等。Tadatsugu Taniguchi等人觀察到在抗病毒應答過程中，一種經過誘導生成的產生干擾素所必需的轉錄因子IRF3，能直接抑制編碼IL-12的基因的轉錄。

除此之外，他們還注意到，就算小鼠體內的細菌數并未達到致死量，病毒感染仍然會通過減弱小鼠的抗菌應答而導致小鼠死亡率上升。這種干擾作用可能有利于保護宿主在抗病毒應答中不產生過多炎癥，卻會在由多種病菌造成的多重感染中產生消極作用。

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.