The functional variant (Asp299gly) of toll-like receptor 4 (TLR4) influences TLR4-mediated cytokine production in rheumatoid arthritis.
until further notice
SourceThe Journal of Rheumatology, 35, 4, (2008), pp. 558-561
Article / Letter to editor
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Scanning Probe Microscopy
The Journal of Rheumatology
SubjectDCN 1: Perception and Action; EBP 1: Determinants in Health and Disease; N4i 1: Pathogenesis and modulation of inflammation; N4i 4: Auto-immunity, transplantation and immunotherapy; NCEBP 2: Evaluation of complex medical interventions; NCMLS 1: Immunity, infection and tissue repair; NCMLS 1: Infection and autoimmunity; Scanning Probe Microscopy; UMCN 4.1: Microbial pathogenesis and host defense; UMCN 4.2: Chronic inflammation and autoimmunity; UMCN 5.1: Genetic defects of metabolism
OBJECTIVE: To investigate functional consequences of the Toll-like receptor 4 (TLR4) variant (Asp299Gly) in rheumatoid arthritis (RA). METHODS: Peripheral blood mononuclear cells from 28 patients with RA carrying or not carrying the TLR4 variant were incubated with lipopolysaccharide (LPS) and heat shock protein B8 (HSPB8). Concentrations of interleukin 6 (IL-6), tumor necrosis factor-alpha(TNF-alpha), and IL-10 were determined along with TLR4 and CD14 expression. RESULTS: TLR4 expression was similar in patients carrying or not carrying the variant. In contrast, both LPS and HSPB8 resulted in significantly lower secretion of IL-6, TNF-alpha, and IL-10 in those who carried the variant, whereas the frequency of CD14+ cells was higher in these individuals. CONCLUSION: TLR4 variant clearly reduces its potency to mediate signaling. Correction for CD14+ cells is necessary in comparable experiments.
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