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Fig. 1. | BMC Biology

Fig. 1.

From: Role of self-organising myddosome oligomers in inflammatory signalling by Toll-like receptors

Fig. 1.

Overview of immune response signalling by Toll-like receptors. Toll-like receptors (TLRs) are present on the cell surface and in endosomes, where they detect microbial cell-wall components, non-self nucleic acids, or danger-associated self molecules. Upon stimulation, TLRs activate pathways that involve myeloid differentiation primary response protein 88 (MYD88) and/or TIR domain-containing adaptor protein inducing IFNβ (TRIF). MYD88 and TRIF nucleate signalling scaffolds, known respectively as myddosomes and triffosomes, that recruit kinases and activate downstream signalling pathways. Crosstalk with other signalling pathways ensures that the TLR signal is properly regulated and leads to apoptosis or cell survival, and the transcription of pro-inflammatory cytokines and chemokines, and type I interferons (IFNs). CD14, a coreceptor for LPS; LBP, LPS-binding protein; LPS, lipopolysaccharide; MAL/TIRAP, MYD88 adaptor-like protein; MD2, myeloid differentiation factor 2; PKCɛ, protein kinase Cɛ; TAK-242, TLR4 inhibitor; TRAM, TRIF-related adaptor molecule. Image and legend adapted from [1]

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