Toll-like receptors in rheumatoid arthritis joint destruction mediated by two distinct pathways

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Abstract
We have shown that RA-SFs maintain their activated phenotype independently of inflammatory cells and cytokines, considering that they invade human cartilage in the severe combined immunodeficiency (SCID) mouse model even in the absence of cytokine producing macrophages and T and B cells.1 By analysing cytokines, matrix degrading enzymes, and signalling molecules in the SCID mouse model, we explored the factors leading to synovial activation.