The role of T-cell interleukin-17 in conducting destructive arthritis: lessons from animal models

Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes. High levels have been detected in the synovial fluid of patients with RA. The trigger for IL-17 is not fully identified; however, IL-23 promotes the production of IL-17 and...

Full description

Saved in:
Bibliographic Details
Published in:Arthritis research & therapy 2005-01, Vol.7 (1), p.29-37
Main Authors: Lubberts, Erik, Koenders, Marije I, van den Berg, Wim B
Format: Article
Language:English
Subjects:
Animals
Antirheumatic Agents - pharmacology
Antirheumatic Agents - therapeutic use
Arthritis, Experimental - drug therapy
Arthritis, Experimental - pathology
Arthritis, Experimental - physiopathology
Arthritis, Rheumatoid - drug therapy
Arthritis, Rheumatoid - etiology
Arthritis, Rheumatoid - pathology
Arthritis, Rheumatoid - physiopathology
Autoimmune Diseases - physiopathology
Bone and Bones - pathology
Carrier Proteins - physiology
Cartilage, Articular - pathology
Cytokines - biosynthesis
Cytokines - genetics
Gene Expression Regulation - physiology
Humans
Inflammation - physiopathology
Interleukin-17 - antagonists & inhibitors
Interleukin-17 - physiology
Interleukins - physiology
Membrane Glycoproteins - physiology
Mice
Neutrophils - pathology
Osteoclasts - pathology
RANK Ligand
Rats
Receptor Activator of Nuclear Factor-kappa B
Receptors, Interleukin - physiology
Receptors, Interleukin-17
Review
Species Specificity
Synovial Fluid - metabolism
T-Lymphocytes - metabolism
Tumor Necrosis Factor-alpha - physiology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes. High levels have been detected in the synovial fluid of patients with RA. The trigger for IL-17 is not fully identified; however, IL-23 promotes the production of IL-17 and a strong correlation between IL-15 and IL-17 levels in synovial fluid has been observed. IL-17 is a potent inducer of various cytokines such as tumor necrosis factor (TNF)-alpha, IL-1, and receptor activator of NF-kappaB ligand (RANKL). Additive or even synergistic effects with IL-1 and TNF-alpha in inducing cytokine expression and joint damage have been shown in vitro and in vivo. This review describes the role of IL-17 in the pathogenesis of destructive arthritis with a major focus on studies in vivo in arthritis models. From these studies in vivo it can be concluded that IL-17 becomes significant when T cells are a major element of the arthritis process. Moreover, IL-17 has the capacity to induce joint destruction in an IL-1-independent manner and can bypass TNF-dependent arthritis. Anti-IL-17 cytokine therapy is of interest as an additional new anti-rheumatic strategy for RA, in particular in situations in which elevated IL-17 might attenuate the response to anti-TNF/anti-IL-1 therapy.
ISSN:1478-6354
1478-6362
DOI:10.1186/ar1478