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Related Experiment Videos

TNF-induced structural joint damage is mediated by IL-1.

Jochen Zwerina¹, Kurt Redlich, Karin Polzer

¹Department of Internal Medicine III, Medical University of Vienna, A-1090 Vienna, Austria.

Proceedings of the National Academy of Sciences of the United States of America

|July 5, 2007

Summary

Interleukin-1 (IL-1) plays a key role in rheumatoid arthritis (RA) cartilage and bone degradation, even when tumor necrosis factor (TNF) is blocked. Removing IL-1 significantly reduces bone erosion and completely prevents cartilage damage in TNF-driven arthritis.

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Area of Science:

Immunology
Rheumatology
Molecular Biology

Background:

Tumor necrosis factor (TNF) blockade effectively treats rheumatoid arthritis (RA), but its precise mechanism, particularly regarding downstream mediators, remains unclear.
Interleukin-1 (IL-1) is implicated in arthritis pathogenesis and is a therapeutic target in human RA.
The exact contribution of IL-1 to TNF-mediated joint destruction needs further elucidation.

Purpose of the Study:

To investigate the role of IL-1 in TNF-induced inflammatory joint disease.
To determine whether IL-1 mediates cartilage and bone erosion in a human TNF-transgenic (hTNFtg) mouse model of arthritis.

Main Methods:

Generation of IL-1-deficient (IL-1-/-) arthritic hTNFtg mice by genetic crossing.
Assessment of synovial inflammation, bone erosion, and osteoclast formation.
Chimera studies to identify the cellular origin of IL-1's protective effects.
Analysis of ADAMTS-5 and MMP-3 expression.

Main Results:

IL-1 deficiency did not significantly affect synovial inflammation in hTNFtg mice.
Bone erosion and osteoclast formation were substantially reduced in IL-1-/-hTNFtg mice, linked to monocyte differentiation defects.
Cartilage damage was completely abolished in IL-1-/-hTNFtg mice.
Protection against cartilage degradation was attributed to IL-1 acting on hematopoietic cells, reducing ADAMTS-5 and MMP-3 expression.

Conclusions:

TNF-mediated cartilage degradation in RA is entirely dependent on IL-1.
TNF-mediated bone degradation in RA is partially dependent on IL-1.
IL-1 is a critical mediator of inflammatory cartilage and bone destruction in the context of TNF-driven arthritis.