Figure 2
From: Negative regulatory approaches to the attenuation of Toll-like receptor signaling
Regulatory checkpoints in the Toll-like receptor (TLR) pathway. Subsequent to stimulation with their cognate ligands, TLRs induce several mediators converging at nuclear factor-κB (NF-κB), which mobilizes the transcription of inflammatory genes. This helps the host prepare to fight the microbial threat. After eliminating the threat, the cell must turn off the expression of inflammatory mediators. Sustained activation and overactivation of TLRs are usually accompanied by deleterious consequences for the host. To prevent these consequences, the cell employs a variety of mechanisms to regulate TLR signaling, including decoy factors, adaptor modification, ubiquitin-mediated degradation, promoter state alteration, and translation disruption. All these mechanisms, individually or in combination, exert the effect of controlling inflammation and supporting the system to regain its normal state (arrows in red indicate the irreversible regulation, whereas the others show the reversible regulation).
