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

Figure 2

TLR signalling inhibitors. The regulation of TLR signalling has been achieved through the application of both natural and synthetic inhibitory molecules, which target each of the key molecules in the TLR signalling pathways, acting through a wide range of mechanisms. (AP-1, activator protein 1; ATF, activating transcription factor; 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; TAB, transforming growth factor-b-activated kinase 1/MAP3K7-binding protein; TAK, transforming growth factor-activated kinase; TRAF, tumour necrosis factor receptor-associated factor); A20, Tumour Necrosis Factor Inducible Protein A20; ATF3, Activating Transcription Factor 3; Bcl-3, B-Cell Lymphoma 3-Encoded Protein; Cbl-b, E3 Ubiquitin Protein Ligase Cbl-b; CYLD, Ubiquitin-Specific-Processing Protease CYLD; DUBA, Deubiquitinating Enzyme A; HA900, high molecular weight hyaluronan; IkBNS, NF-κB Inhibitor Delta; Nurr1, Nuclear Receptor Related 1; PDLIM2, PDZ and LIM Domain Protein 2; PIN1, Peptidylprolyl Cis/Trans Isomerase, NIMA-Interacting 1; SARM, Sterile Alpha and TIR Motif Containing 1; SHP, Small Heterodimer Partner; SOCS1, Suppressor of Cytokine Signalling 1; SOCS3, Suppressor of Cytokine Signalling 3; TAG, splice variant of the adaptor TRAM; TANK, TRAF Family Member Associated NF-κB Activator; TRIM5, Tripartite Motif Containing 5; TRIM38, Tripartite Motif Containing Protein 38; UBE3C, Ubiquitin Protein Ligase E3C; USP4, Ubiquitin Specific Peptidase 4.