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. 2009 Nov 4;30(7):830–882. doi: 10.1210/er.2009-0013

Figure 1.

Figure 1

Inflammation at a molecular level: a simplified scheme. TNFR activation by TNF, IL1RI by IL1β, TLR3 by double-stranded RNA (dsRNA), TLR4 by bacterial LPS, and activation of other TLRs can signal via specific intermediary factors such as TRADD, TRAF2, RIP1, MEKK3, TAK1, TAB2/3, and NIK (for the TNFR), MyD88, IRAKs, TRAF6 and TAK1 (for IL1RI), Trif, RIP1, TRAF6 and TAK1 (for TLR3) and MyD88, Mal, Trif, Tram, RIP1, IRAKs, TRAF6 and TAK1 (for TLR4) to the MAPK pathway and to the activation and regulation of NF-κB and AP-1. Additionally, triggering TLR3 or TLR4 signaling cascades can instigate IKKε and TBK1 activation and subsequent IRF3-regulated gene transcription (10,11,12,29). TAB, TAK1-binding protein.