Our findings indicate that TLR-3 and TLR-7 are expressed in inflammatory myopathic tissues, particularly in immature myoblast precursors. Necrotic muscle cells activate cytokine production, in part, through the TLR-3 pathway, with a differential regulatory effect of Th1 and Th17 cytokines.[1]

Toll-like receptors (TLRs) are key sentinels that link innate and adaptive immunity. TLRs mediate inflammatory stimuli from pathogens and endogenous danger signals, including bacterial cell components, bacterial DNA, or viral RNA. TLR-1, TLR-2, TLR-4, and TLR-6 recognize lipid-based pathogen-associated molecular patterns (PAMPs), whereas TLR-3, TLR-7, TLR-8, and TLR-9 recognize nucleic acid–based PAMPs. TLR activation leads to the generation of cytokines and chemokines and to the maturation of antigen-presenting cells (APCs) by up-regulating costimulatory molecules that promote efficient interactions between APCs and T cells. The recent identification of endogenous ligands for TLR-3 and TLR-7, such as RNA, suggests that TLRs may be involved in autoimmune disease pathogenesis [1]

 

Tournadre, A., Lenief, V. and Miossec, P. (2010), Expression of toll-like receptor 3 and toll-like receptor 7 in muscle is characteristic of inflammatory myopathy and is differentially regulated by Th1 and Th17 cytokines. Arthritis & Rheumatism, 62: 2144–2151. doi:10.1002/art.27465