title: Innate recognition of intracellular bacteria.
abstract: The molecular repertoire for innate recognition of bacterial pathogens has expanded rapidly in the past decade. These immunosensors include Toll-like receptors and the more recently defined NOD-like receptors (NLRs): NODs, NALPs, NAIP and IPAF. Toll-like receptors signal from the cell surface or endosome upon ligand binding, whereas NLRs are activated by characteristic bacterially derived molecules, such as peptidoglycan, RNA, toxins and flagellin, in the cytosol. Studies using animal and culture models of bacterial infection indicate a pro-inflammatory role for NLRs, mediated by signaling through nuclear transcription factor kappaB and activation of caspase-1 by the inflammasome. These data also support a synergistic role for extracellular and intracellular bacterial sensing in regulating inflammation. In humans, NLR mutations are often associated with autoinflammatory syndromes, suggesting a complex role for cytosolic surveillance in systemic innate immunity.
authors.affiliation: Department of Microbiology and Immunology, University of Michigan Medical School, 1150W Medical Center Drive, 5641 Medical Sciences II, Ann Arbor, MI 48109-0620, USA.
authors.forename: Laura M
authors.initials: LM
authors.lastname: Delbridge
authors.forename: Mary X D
authors.initials: MX
authors.lastname: O'Riordan
mesh_terms: D000818:Animals; D001419:Bacteria / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D007424:Intracellular Fluid / Q000276:immunology* / Q000382:microbiology*; D016952:Legionella pneumophila / Q000276:immunology; D009169:Mycobacterium tuberculosis / Q000276:immunology; D012486:Salmonella typhimurium / Q000276:immunology