Figure 1.

Schematic expression of several PAMP and DAMP signals. TLR and IL-1 R usually share a common signaling event. PAMP and DAMP bind to corresponding ligands, TLR dimer forms a homodimer or heterodimer, and conformational changes occur. MyD88 was the first adaptor molecule to be identified and is involved in all TLR (except TLR3)-induced signal transduction.MyD88 relies on a pathway to initiate a series of events that lead to the activation of IRAK kinase, which leads to the activation of NF-κB transcription factor and the expression of the pro-validation factor gene. In response to TLR stimulation, the MYD88-dependent pathway also activates the interferon regulatory factor (IRF) family of transcription factors IRF1, IRF5, or IRF7 phosphorylation mecha-intensity, which lead to formation of their translocated nuclei and bind to target interferon stimulation-responsive elements (ISRES) with the transcription co-activators association. IRF1 and IRF7 are involved in transcriptional control of type I interferon, while IRF5 is involved in the transcription of all pro-inflammatory cytokines tested to date by TLRs.