IL-18 Upregulates the Production of Key Regulators of Osteoclastogenesis from Fibroblast-Like Synoviocytes in Rheumatoid Arthritis

[1]  A. Koch,et al.  Interleukin-18: a mediator of inflammation and angiogenesis in rheumatoid arthritis. , 2011, Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research.

[2]  H. Kitaura,et al.  IL-18 Inhibits TNF-α-Induced Osteoclastogenesis Possibly via a T Cell-Independent Mechanism in Synergy with IL-12 In Vivo , 2010, Calcified Tissue International.

[3]  A. Koch,et al.  Interleukin-18 induces angiogenic factors in rheumatoid arthritis synovial tissue fibroblasts via distinct signaling pathways. , 2007, Arthritis and rheumatism.

[4]  Huji Xu,et al.  Cellular targets of interleukin-18 in rheumatoid arthritis , 2007, Annals of the rheumatic diseases.

[5]  G. Schett.  Cells of the synovium in rheumatoid arthritis. Osteoclasts , 2007, Arthritis research & therapy.

[6]  G. Burmester,et al.  Cells of the synovium in rheumatoid arthritis , 2007 .

[7]  Claudia Mauri,et al.  Cells of the synovium in rheumatoid arthritis , 2007 .

[8]  D. Jue,et al.  Interleukin-18 induces the production of vascular endothelial growth factor (VEGF) in rheumatoid arthritis synovial fibroblasts via AP-1-dependent pathways. , 2006, Immunology letters.

[9]  B. Möller.  Interleukin-18 receptor expression in synovial fluid-derived fibroblast-like synoviocytes: comment on the article by Kawashima and Miossec. , 2004, Arthritis and rheumatism.

[10]  K. Migita,et al.  Interleukin-18 induces serum amyloid A (SAA) protein production from rheumatoid synovial fibroblasts. , 2004, Life sciences.

[11]  K. Yudoh,et al.  Interleukin (IL) 18 stimulates osteoclast formation through synovial T cells in rheumatoid arthritis: comparison with IL1 beta and tumour necrosis factor alpha. , 2004, Annals of the rheumatic diseases.

[12]  David L. Lacey,et al.  Osteoclast differentiation and activation , 2003, Nature.

[13]  P. Miossec,et al.  Heterogeneity of response of rheumatoid synovium cell subsets to interleukin-18 in relation to differential interleukin-18 receptor expression. , 2003, Arthritis and rheumatism.

[14]  Pawan Kumar,et al.  Signal Transduction Pathways Involved in Rheumatoid Arthritis Synovial Fibroblast Interleukin-18-induced Vascular Cell Adhesion Molecule-1 Expression* , 2002, The Journal of Biological Chemistry.

[15]  S. Rehart,et al.  Expression of interleukin-18 receptor in fibroblast-like synoviocytes , 2001, Arthritis research.

[16]  Pawan Kumar,et al.  Interleukin-18 Induces Rheumatoid Arthritis Synovial Fibroblast CXC Chemokine Production through NFκB Activation , 2001, Laboratory Investigation.

[17]  N. Athanasou,et al.  The effect of macrophage-colony stimulating factor and other humoral factors (interleukin-1, -3, -6, and -11, tumor necrosis factor-alpha, and granulocyte macrophage-colony stimulating factor) on human osteoclast formation from circulating cells. , 2001, Bone.

[18]  I. McInnes,et al.  Reduced Incidence and Severity of Collagen-Induced Arthritis in Mice Lacking IL-181 , 2001, The Journal of Immunology.

[19]  R. Gay,et al.  Expression of osteoclast differentiation factor in rheumatoid arthritis. , 2000, Arthritis and rheumatism.

[20]  D. Murray,et al.  Rheumatoid arthritis synovial macrophage–osteoclast differentiation is osteoprotegerin ligand‐dependent , 2000, The Journal of pathology.

[21]  Kozo Nakamura,et al.  Involvement of receptor activator of nuclear factor kappaB ligand/osteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis. , 2000, Arthritis and rheumatism.

[22]  S. Goldring,et al.  Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor. , 2000, Arthritis and rheumatism.

[23]  I. McInnes,et al.  A proinflammatory role for IL-18 in rheumatoid arthritis. , 1999, The Journal of clinical investigation.

[24]  Y. Oike,et al.  Granulocyte/macrophage colony-stimulating factor and interleukin-3 correct osteopetrosis in mice with osteopetrosis mutation. , 1999, The American journal of pathology.

[25]  T. Thornhill,et al.  Identification of cell types responsible for bone resorption in rheumatoid arthritis and juvenile rheumatoid arthritis. , 1998, The American journal of pathology.

[26]  H. Okamura,et al.  Interleukin 18 inhibits osteoclast formation via T cell production of granulocyte macrophage colony-stimulating factor. , 1998, The Journal of clinical investigation.

[27]  H. Okamura,et al.  Interleukin-18 (interferon-gamma-inducing factor) is produced by osteoblasts and acts via granulocyte/macrophage colony-stimulating factor and not via interferon-gamma to inhibit osteoclast formation. , 1997 .

[28]  F. Arnett.  Revised criteria for the classification of rheumatoid arthritis. , 1990, Orthopedic nursing.

[29]  S. Jonjić,et al.  Site-restricted persistent cytomegalovirus infection after selective long-term depletion of CD4+ T lymphocytes , 1989, The Journal of experimental medicine.

[30]  M. Liang,et al.  The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. , 1988, Arthritis and rheumatism.