TLR signaling

• Published in: Cell death and differentiation Vol. 13; no. 5; pp. 816 - 825
• Main Authors: Kawai, T, Akira, S
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 01.05.2006
• Subjects: Adapter proteins; Adaptive immunity; Adaptor Proteins, Signal Transducing - metabolism; Adaptor Proteins, Vesicular Transport - metabolism; Animals; Bacteria; Cell death; Cytokines; DEAD-box RNA Helicases; Drosophila; Gene Expression Regulation; Gram-positive bacteria; Humans; Immunity, Innate; Insects; Interferon; Interferon Regulatory Factors - metabolism; Interferon-Induced Helicase, IFIH1; Kinases; Membrane Proteins - metabolism; Mice; Models, Biological; Mutation; Myeloid Differentiation Factor 88; Nerve Tissue Proteins - metabolism; NF-kappa B - metabolism; Pathogens; RNA Helicases - metabolism; Signal Transduction; Toll-Like Receptors - metabolism; Transcription Factor AP-1 - metabolism; Tumor necrosis factor-TNF; Viruses; Japan
• ISSN: 1350-9047; 1476-5403
• DOI: 10.1038/sj.cdd.4401850

The Toll-like receptor (TLR) family plays an instructive role in innate immune responses against microbial pathogens, as well as the subsequent induction of adaptive immune responses. TLRs recognize specific molecular patterns found in a broad range of microbial pathogens such as bacteria and viruses, triggering inflammatory and antiviral responses and dendritic cell maturation, which result in the eradication of invading pathogens. Individual TLRs interact with different combinations of adapter proteins and activate various transcription factors such as nuclear factor (NF)-kappaB, activating protein-1 and interferon regulatory factors, driving a specific immune response. This review outlines the recent advances in our understanding of TLR-signaling pathways and their roles in immune responses. Further, we also discuss a new concept of TLR-independent mechanisms for recognition of microbial pathogens.