[Molecular mechanisms of bone destruction in rheumatoid arthritis].
Osteoclast in the synovium of rheumatoid arthritis (RA) plays an important role for bone destruction of the affected joints. The osteoclast is differentiated from macrophage-like synoviocyte, which is migrated from peripheral blood monocytes. In the RA synovium, receptor activator of NF-kappaB ligand (RANKL) which is expressed by T cells and fibroblast-like synoviocytes (FLS) and macrophage colony-stimulating factor (M-CSF) which is expressed by FLS induce the differentiation into osteoclast from macrophage-like synoviocyte. TNF-alpha, interleukin (IL) -1, IL-6, and IL-17 which are expressed by macrophages, FLS, and/or T cells in the synovium enhance the differentiation and activation of the osteoclast. Thus, such synovial cells contribute osteoclastgenesis and bone destruction.
Nanki
Toshihiro
T
Tokyo Medical and Dental University, Department of Medicine and Rheumatology.
D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000473:pathology*; D001842:Bone and Bones / Q000473:pathology*; D002454:Cell Differentiation / Q000235:genetics* / Q000276:immunology; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology; D020381:Interleukin-17 / Q000502:physiology; D015850:Interleukin-6 / Q000502:physiology; D016173:Macrophage Colony-Stimulating Factor / Q000502:physiology; D010010:Osteoclasts / Q000166:cytology*; D053245:RANK Ligand / Q000502:physiology; D013583:Synovial Membrane / Q000166:cytology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D007375:Interleukin-1; D020381:Interleukin-17; D015850:Interleukin-6; D053245:RANK Ligand; D014409:Tumor Necrosis Factor-alpha; D016173:Macrophage Colony-Stimulating Factor