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. 2021 Nov 19;9(11):e003065. doi: 10.1136/jitc-2021-003065

Figure 2.

Figure 2

Classical TLR signaling pathways in human innate immune cells. TLR molecules can signal through MyD88-dependent and independent pathways. In the MyD88-dependent pathway, activation of proinflammatory transcription factors AP1 and NF-kB is induced via IRAK1/4, TRAF6 and TAK1. In the MyD88-independent pathway, the adaptor molecule TRIF initiates signaling via TRAF3 and IRF, also resulting in the induction of proinflammatory gene transcription. AP1, activator protein 1; IRAK, IL-1R-associated kinase; IRF, interferon-regulatory factor; LPS, lipopolysaccharide; MyD88, myeloid Differentiation Primary Response 88; NF-kB, nuclear factor kappa B; TAK1, transforming growth factor-β-activated kinase-1; TIRAP, toll-IL 1 receptor domain containing adaptor protein; TLR, toll-like receptor; TRAF, tumor necrosis factor receptor-activated factor; TRAM, TRIF-related adaptor molecule; TRIF, toll/IL-1R domain-containing adaptor-inducing IFN-β.