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2004, Progress in inflammation research, ISBN 3764370017, xi, [296]
Book
1998, PIR, progress in inflammation research., ISBN 9783764358532, xii, 236
Book
Rheumatology, ISSN 1462-0324, 03/2019, Volume 58, Issue 3, pp. 536 - 546
Abstract Objective To investigate the role of AXL, a member of the anti-inflammatory TYRO3, AXL MER (TAM) receptor family, in arthritis. Methods KRN serum... 
Knee | Phenotypes | Transforming growth factor-b1 | Arthritis | Inflammation | Gene expression | Gene deletion | Macrophages | Joint diseases | Synovium | Axl protein | Ankle | Clonal deletion | Fibroblasts | Protein-tyrosine kinase receptors
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 03/2017, Volume 76, Issue Suppl 1, pp. A62 - A62
BackgroundNo disease-modifying drugs are available for osteoarthritis (OA). Although the aetiology is still unknown, inflammation is indicated to be involved... 
Journal Article
Rheumatology (Oxford, England), ISSN 1462-0324, 04/2018, Volume 57, Issue 4, p. 737
Objectives: RA is a chronic autoimmune disease leading to progressive destruction of cartilage and bone. RA patients show elevated IL-22 levels and the amount... 
therapy monitoring | anti-FAP | anti-IL-22 | experimental arthritis | SPECT/CT
Journal Article
Cell and Tissue Research, ISSN 0302-766X, 01/2014, Volume 355, Issue 1, pp. 163 - 171
Lysyl hydroxylase 2b (LH2b) is known to increase pyridinoline cross-links, making collagen less susceptible to enzymatic degradation. Previously, we observed a... 
PATHWAYS | HUMAN-DISEASE | INDUCTION | Synovium | OSTEOPHYTE FORMATION | OVEREXPRESSION | TGF-beta | GROWTH-FACTOR-BETA | Fibrosis | Lysyl hydroxylase 2b | Osteoarthritis | EXPRESSION | PYRIDINOLINE CROSS-LINKS | TRANSIENT FIBROSIS | TGF-BETA-1 | CELL BIOLOGY | Collagen | Analysis | Heat shock proteins | Bone morphogenetic proteins | Hydroxylases | Transforming growth factors | Gene expression
Journal Article
Rheumatology (United Kingdom), ISSN 1462-0324, 01/2018, Volume 57, Issue 4, pp. 737 - 747
Objectives. RA is a chronic autoimmune disease leading to progressive destruction of cartilage and bone. RA patients show elevated IL-22 levels and the amount... 
Anti-FAP | Experimental arthritis | Pharmacology (medical) | Rheumatology | UT-Hybrid-D | Anti-IL-22 | SPECT/CT | Therapy monitoring
Journal Article
Arthritis & Rheumatology, ISSN 2326-5191, 04/2016, Volume 68, Issue 4, p. 795
Objective The prevalence of periodontitis is increased in patients with rheumatoid arthritis (RA), and the severity of periodontitis can affect the level of... 
Immunology | Research Support, Non-U.S. Gov't | Rheumatology | Immunology and Allergy | Journal Article
Journal Article
Arthritis Research & Therapy, ISSN 1478-6354, 2005, Volume 7, Issue 1, pp. 29 - 37
Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes. High levels have been detected... 
Inflammation | Osteoclast | Autoimmune diseases | Interleukin-23 | Receptor activator of NF-κB ligand | Cytokine | autoimmune diseases | cytokine | RHEUMATOID-ARTHRITIS | COLLAGEN-INDUCED ARTHRITIS | BONE EROSION | NECROSIS-FACTOR-ALPHA | RHEUMATOLOGY | receptor activator of NF-kappa B ligand | interleukin-23 | NITRIC-OXIDE PRODUCTION | MESSENGER-RNA | inflammation | ARTICULAR-CARTILAGE | IN-VIVO | HUMAN OSTEOARTHRITIC CHONDROCYTES | osteoclast | NF-KAPPA-B | Autoimmune Diseases - physiopathology | Bone and Bones - pathology | Arthritis, Experimental - drug therapy | Receptor Activator of Nuclear Factor-kappa B | Species Specificity | Humans | Interleukin-17 - physiology | Synovial Fluid - metabolism | RANK Ligand | Receptors, Interleukin-17 | Arthritis, Experimental - pathology | Membrane Glycoproteins - physiology | Interleukins - physiology | Arthritis, Rheumatoid - drug therapy | Antirheumatic Agents - pharmacology | Cytokines - genetics | Arthritis, Rheumatoid - physiopathology | Antirheumatic Agents - therapeutic use | Neutrophils - pathology | Carrier Proteins - physiology | Osteoclasts - pathology | Receptors, Interleukin - physiology | T-Lymphocytes - secretion | Arthritis, Experimental - physiopathology | Arthritis, Rheumatoid - etiology | Gene Expression Regulation - physiology | Rats | Arthritis, Rheumatoid - pathology | Cartilage, Articular - pathology | Animals | Interleukin-17 - antagonists & inhibitors | Tumor Necrosis Factor-alpha - physiology | Mice | Cytokines - biosynthesis | Inflammation - physiopathology | receptor activator of NF-κB ligand | Review
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 03/2014, Volume 73, Issue Suppl 1, pp. A68 - A69
Background and Objectives Rheumatoid arthritis (RA) is a chronic destructive autoimmune disease with periods of exacerbation and remission. An attractive... 
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 03/2013, Volume 72, Issue Suppl 1, pp. A15 - A15
Background and Objectives Both IL-6 and IL-21 have been described to drive in vitro Th17 differentiation in the presence of TGFbeta. We explored whether also... 
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 03/2014, Volume 73, Issue 3, p. A9
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 03/2014, Volume 73, Issue Suppl 1, pp. A24 - A24
Background and Objective T helper-17 (Th17) cells are important mediators of inflammatory diseases, and are the main pathogenic cell type in many animal models... 
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 03/2013, Volume 72, Issue Suppl 1, pp. A46 - A46
Background and Objectives Local gene therapy for arthritis, with the use of disease-inducible promoters, represents a promising alternative for coping with... 
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 03/2014, Volume 73, Issue Suppl 1, pp. A69 - A69
Background and Objectives Gene therapy applied in the joints of rheumatoid arthritis (RA) patients can provide a local production of biological drugs to... 
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 02/2012, Volume 71, Issue Suppl 1, pp. A74 - A75
Background and objectives The IL-1 receptor antagonist knockout mice (IL-1Ra-/-) spontaneously develop a T cell driven arthritis with profound IL-17... 
Journal Article
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