Abstract
The innate immune system represents a critical, first-line response to infection and injury. Innate responses are most commonly initiated through pattern recognition receptors (PRRs) upon interactions with conserved components expressed by microbes. The signaling that ensues ultimately leads to various antimicrobial and inflammatory gene products. The downstream outcomes of PRR signaling can be time-, location-, and cell type-dependent. The regulation of PRR-initiated signaling pathways is particularly critical in the intestinal immune system, where innate cells are continuously interacting with the high density of resident microbiota in the intestinal lumen. Consistently, a number of the genes implicated in human inflammatory bowel disease regulate innate immune responses, and perturbations in PRR signaling pathways in mice can lead to increased susceptibility to intestinal microbes and/or intestinal inflammation. Future studies examining tissue- and context-specific features of innate immune cell signaling will provide a deeper understanding of mechanisms shaping immune function at mucosal surfaces.
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