[Toll-like receptor].

By K. Takeda. Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology, 2005

875 citations recorded by the source corpus.

Toll-like receptors (TLRs) have been revealed to recognize specific patterns of microbial components. Recognition of microbial components by TLRs initiates signal transduction pathways, triggering expression of genes, which products control innate immune responses and further instruct development of antigen-specific acquired immunity. TIR domain-containing adaptors, such as MyD88, TIRAP, TRIF, and TRAM, play pivotal roles in TLR signaling pathways. Differential utilization of these TIR domain-containing adaptors provides specificity of individual TLR-mediated signaling pathways. TLR-mediated activation of innate immunity, when in excess, leads to immune disorders such as inflammatory bowel diseases. Therefore, several mechanisms that negatively control TLR signaling pathways and thereby prevent overactivation of innate immunity have been elucidated. Nuclear IkappaB proteins, such as Bcl-3 and IkappaBNS, have been revealed to be responsible for this process, by differentially inhibiting TLR-dependent cytokine production.

Subfields: Immunology, Small Animals

View Paper: https://www.semanticscholar.org/paper/2b0754941b3f306fe922d998fc1618fb8ac97d83

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In Immunology

Citations in the corpus

The Role of TLR2 in Infection and Immunity (2012, background): “Studies with TLR2 knockout mice showed both resistance (Netea et al., 2004b) or susceptibility to primary or secondary systemic C. albicans infection (Gil et al., 2005; Hise et al., 2009), while TLR2 knockout macrophages showed impaired fungal clearance (Blasi et al., 2005), with both impairment or…”
Microglia Polarization From M1 to M2 in Neurodegenerative Diseases (2022, background): “Ma et al. (2020) found that autophagy was associated with TLR2 signaling, and TLR2-mediated autophagy could regulate microglial M1/M2 phenotype switching.”