Figure 1

From: Toll-like receptors: potential targets for lupus treatment

Figure 1

Potential targets involved in TLR signaling pathways for SLE treatment. TLR-mediated responses are controlled mainly in a MyD88-dependent way, which is used by all TLRs except TLR3. In the pathogenesis of SLE, both exogenous ligands from infection and endogenous ligands from apoptotic debris contribute to the activation of TLRs and initiate the downstream signaling cascade, resulting in the production of type I IFN and inflammatory cytokines. A series of potential therapeutics, including oligonucleotides, SMIs and antibodies, modulate TLR signaling pathways at different stages. Some oligonucleotides, SMIs and TLR-neutralized antibodies directly block TLRs; some SMIs target TLR accessory proteins, such as MyD88 and IRAKs. Anti-IFN-α antibodies are also under intensive development for the treatment of SLE. TAK1, transforming growth factor-β-activated kinase; IRF, interferon regulatory factor.