The role of galectin-3 and galectin-9 in the chronic inflammation of rheumatoid arthritis

摘要: Fibroblasts are important regulators of inflammatory processes. The phenotype fibroblasts differ according to anatomical site which may dtermine immune functions such as leukocyte accumulation and predilection for disease in certain tissues. This thesis describes the expression profile explores function a family immunomodulatory proteins (galectins) from rhematoid arthritis patients. Synovial were found significantly bone marrow skin with higher galectin-9 galectin-12 synovial fibroblasts. Galectin-9 galectin-3 was also examined situ tissue rheumatoid (RA) osteoarthritis (OA) Expression both galectins RA compared OA but not cultured vitro. Galectin-3 seemed be controlled by epigenetic factors (methylation) cytokine stimulation. production up-regulated interferon-y, interleukin-1b ligands Toll-like receptors 3 (TLR3) 4 (TLR4). It that intracellular presence firboblasts increased their resistance apoptosis. level teh joints patients arthritis. Studies on effect mechanism action revealed exogenously added induced cytokines (IL-6) moncyte attracting chemokines (CCL5, CCL2) uniquely derived synovium. Different signalling pathways mediated secretion those mediators. IL-6 release depended MAP kinases p38, ERK JNK well NFkB transcription factor, whereas CCL5 required PI3/Akt