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Activation of the innate immune system via Toll-like receptors (TLRs) is considered to play an important role in the propagation of the inflammatory response in rheumatoid arthritis (RA) patients. In macrophages, repeated stimulation of TLR pathways with LPS leads to a tolerant state of the cell, protecting inflamed tissues from inflammation-induced damage. We hypothesized that a lack of tolerizable effects in stromal cells significantly contributes to sustained inflammation and inflammation-induced damage seen in RA.

To investigate tolerizable and non-tolerizable effects in RA synovial fibroblasts (RASF) after TLR stimulation compared to macrophages.

RASF and in vitro differentiated peripheral blood derived macrophages from healthy donors were treated with the TLR4 agonist LPS (100 ng/ml). 24h after the initial stimulation, cells were washed and re-stimulated with 1/10 of the …