The Role of Toll-Like Receptors in Autoimmune Diseases through Failure of the Self-Recognition Mechanism

Figure 1

TLR signalling pathways. The two main pathways by which TLR signalling occurs upon stimulation by their ligands. These pathways are characterised depending on which of the adaptor molecules MyD88 or TRIF are involved. These signalling cascades result in the activation of NF-kB, IRFs, and MAP kinases, which promote the transcription of various immune response genes, including inflammatory cytokines and IFNγ-related genes. (AP-1, activator protein 1; ERK, extracellular signal-regulated kinase; IKK, inhibitor of kappa light polypeptide gene enhancer in B-cell kinase; IRAK, IL-1 receptor-associated kinase; JNK, c-Jun N-terminal kinase; MKK, MAPK kinase; RIP1, receptor interacting protein 1; TAK, transforming growth factor-activated kinase; TBK1, TANK-binding kinase 1; TRAF, tumour necrosis factor receptor-associated factor.)