Figure 1.

TLR molecular cascade. Upon activation, TLRs can signal through different transduction molecules. The MyD88-mediated pathway constitutes the classical TLR signaling pathway and ultimately leads to the activation of the NF-κB transcription factor, resulting in the production and release of pro-inflammatory mediators. In addition, some members of the TLR family can activate other pathways, such as PI3K and JAK/STAT. Although these mechanisms also lead to NF-κB activation, the intermediary molecular nodes can interact and activate additional signaling pathways. TLR, toll-like receptor; MyD88, myeloid differentiation factor 88; TAK1, transforming growth factor-β-activated kinase-1; IKK, inhibitory NF-κB kinases; NLK, nemo-like kinase; JNK, c-Jun N-terminal kinases; NF-κB, nuclear factor-κB; TRIF, TIR-containing adaptor inducing interferon-β; PI3K, phosphatidylinositide-3 kinase; Akt, protein kinase B; GSK3β, glycogen synthase kinase 3 β; JAK, Janus kinase; STAT, signal transducer and activator of transcription.