ABSTRACT
Introduction Non-self recognition of an invading microbial pathogen is a first and critical step in programming
the host immune system for control of infection. Mammalian cells recognize microbial invaders through the actions of a wide variety of pathogen recognition receptor (PRR) molecules. PRRs serve to distinguish self from non-self by virtue of their recognition of and interaction with pathogen-specific macromolecules, termed pathogen associated molecular patterns (PAMPs).1 Human cells variably express a variety of PRRs, including the RIG-I like receptors (RLRs), Toll-like receptors (TLRs), NOD-like receptors (NLRs), as well as other less defined sensors (such as those responsible for sensing cytoplasmic DNA, specific carbohydrates, and certain lipids).14 Differential compartmentalization of PRRs, as well as their cell-specific expression, creates a comprehensive and complex network for PAMP sensing dedicated to immune signaling. PAMPs encompass a wide range of moieties, including protein, nucleic acids, lipids, and certain carbohydrates or combinations of each, that harbor structural signatures of a particular pathogen or group of pathogens. These molecules differ from host cell macromolecules sufficiendy in structure, location, and/or interactions such that they are discriminated as non-self through PRR interaction. Non-self recognition and PAMP binding by PRRs leads to the rapid engagement of downstream intracellular signaling cascades that activate a variety of host transcription factors. This process lead to alteration of host cell gene expression and induction of intracellular immune defenses termed the innate immune response. In terms ofvirus infection, this response drives the expression of a variety of genes
Nucleic Acid Sensors and Antiviral Immunity, edited by Suryaprakash Sambhara and Takashi Fujita. ©2013 Landes Bioscience.
