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Infections can cause a multitude of stresses on the host and microbe. To detect potential infections, the mammalian immune system utilizes several families of pattern recognition receptors, which survey the intracellular and extracellular environments for microbial products. Members of each receptor family induce antimicrobial effector responses, which include inflammatory cytokine or interferon expression, downregulation of protein synthesis, or host cell death. In this review, we discuss the benefits of each of these innate immune responses. We highlight how non-infectious bacteria and viruses typically activate a single family of receptors, which results in a predictable host response. Infections with virulent pathogens, in contrast, may activate receptors from distinct families. As each receptor family may induce responses that antagonize or synergize with the activities of another family, cell fate decisions during pathogenic encounters are unpredictable. Understanding the antagonistic antimicrobial activities of the innate immune system should provide insight into how cell fate decisions are made during infections and potentially during other environmental stresses. [ABSTRACT FROM AUTHOR]

To prevent the spread of infection, an invading pathogen must first be recognized by the innate immune system. Host pattern recognition receptors detect distinct pathogen-associated molecules and induce the transcription and release of interferon and inflammatory molecules to resolve infection. Unlike infections with pathogens that replicate autonomously from the host, viral infections blur the boundaries of self and non-self. Differentiation of host from virus is achieved by restricting localization of host nucleic acids and by placing pattern recognition receptors in specific subcellular compartments. Within this review, we discuss how several families of pattern recognition receptors act to provide a comprehensive surveillance network that has the potential to induce interferon expression in response to any viral infection. [ABSTRACT FROM AUTHOR]