Science · 1999 · 1.5K citations · 19 references
Life SciencesImmunologyMicrobiologyApoptosisInflammationInnate ImmunityInflammatory SignalingInnate Immune ActivationInnate Immune ReceptorsInnate Immune ResponseInnate Immune Signaling PathwaysToll-like ReceptorsAntibacterial Innate SignalingHost Defense ProteinsLipopolysaccharide-mediated PathogenesisNuclear Factor Kappa B ActivationRespiratory Burst EffectsToll-like Receptor SignalingToll-like Receptor Signaling PathwaysToll-like Receptor-mediated Innate Immune Response
Apoptosis contributes to inflammation initiated by bacterial pathogens, whose lipoproteins activate innate immunity. BLPs trigger apoptosis and stimulate NF‑κB and respiratory burst in hTLR2‑expressing cells, linking microbial products, apoptosis, and host defense.
Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor–2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor–κB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.
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Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in <i>Tlr4</i> Gene
Alexander Poltorak, Xiaolong He, Irina Smirnova et al. · Science · 1998 · 7.6K citations
Host Defense Mechanisms Triggered by Microbial Lipoproteins Through Toll-Like Receptors
Hans D. Brightbill, Daniel H. Libraty, Stephan R. Krutzik et al. · Science · 1999 · 1.7K citations
Toll-like receptor-2 mediates lipopolysaccharide-induced cellular signalling
Ruey‐Bing Yang, Melanie R. Mark, Alane Gray et al. · Nature · 1998 · 1.2K citations