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. 2007 Apr;88(2):85–94. doi: 10.1111/j.1365-2613.2006.00507.x

Figure 1.

Figure 1

Schematic illustration of the co-ordinated activation of pro-inflammatory signalling pathways by TLR ligands and the pro-inflammatory cytokines TNFα, IL-1 and IFN. Adaptor molecules (MyD88, TRADD and TRAF) and receptor associated kinases (RIP, IRAK and JAK) couple to downstream kinase cascades (MAPK; JNK, p38; TAB/TAK, IKK) which regulate the activation of transcription factors (AP-1, NF-κB, CREB and STAT) and the expression of pro-inflammatory genes. A number of negative regulatory mechanisms (shown in red) limit the activation of specific signalling pathways; SOCS targets JAK/STAT and TLR signalling; PTEN and SHIP phosphatases block PI3K; A20 and IKKα negatively regulate the NF-κB pathway; the MAPK phosphatase MKP limits activation of JNK and p38.