Objective Toll-like receptors (TLR) mediate cell activation on stimulation with microbial constituents, being considered as an important link between innate and adaptive immune response. For signal transduction they share the nuclear factor kappa B pathway, similar to proinflammatory cytokine receptors. Inflammatory cytokines regulate their expression. Thus, TLR are also supposed to play a role in the pathogenesis of autoimmune diseases.
Methods In the present work we studied the cellular expression of TLR2 (Gram-positive trigger) and TLR4 (Gram-negative trigger) in patients with juvenile idiopathic arthritis (n = 151) and systemic autoimmune diseases (n = 132) compared with healthy controls (n = 118). Blood-derived monocytes were stained with commercially available monoclonal antibodies for human TLR2 and TLR4, followed by flowcytometric analysis and computer supported evaluation.
Results We were able to demonstrate that TLR4 but not TLR2 expression was significantly elevated in patients with juvenile idiopathic arthritis (JIA), especially during the acute phase of the disease and mainly in patients with arthritis when compared with healthy controls. In contrast, in systemic JIA and systemic lupus erythematosus upregulation of TLR4 did not occur, whereas TLR2 expression was significantly depressed.
Conclusions The role of TLR to promote an autoimmune inflammatory host response to an infectious trigger (ie, superantigen) is discussed. The question whether genetic TLR polymorphism contributes to the development of JIA is under investigation.
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